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Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy
Open accessAbstract
Physicians think of mast cells and IgE primarily in the context of allergic disorders, including fatal anaphylaxis. This 'bad side' of mast cells and IgE is so well accepted that it can be difficult to think of them in other contexts, particularly those in which they may have beneficial functions. However, there is evidence that mast cells and IgE, as well as basophils (circulating granulocytes whose functions partially overlap with those of mast cells), can contribute to host defense as components of adaptive type 2 immune responses to helminths, ticks and certain other parasites. Accordingly, allergies often are conceptualized as "misdirected" type 2 immune responses, in which IgE antibodies are produced against any of a diverse group of apparently harmless antigens, and against components of animal venoms. Indeed, certain unfortunate patients who have become sensitized to venoms develop severe IgE-associated allergic reactions, including fatal anaphylaxis, upon subsequent venom exposure. In this review, we will describe evidence that mast cells can enhance innate resistance, and survival, to challenge with reptile or arthropod venoms during a first exposure to such venoms. We also will discuss findings indicating that, in mice surviving an initial encounter with venom, acquired type 2 immune responses, IgE antibodies, the high affinity IgE receptor (FcεRI), and mast cells can contribute to acquired resistance to the lethal effects of both honeybee venom and Russell's viper venom. These findings support the hypothesis that mast cells and IgE can help protect the host against venoms and perhaps other noxious substances.
Overview
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TL;DR
This review argues that mast cells and IgE, best known for allergic pathology, can also enhance innate and acquired resistance to animal venoms in mice. It synthesizes evidence that mast-cell proteases detoxify some venom components and that IgE/FcεRI/mast-cell responses can protect against honeybee and Russell’s viper venom, while noting unresolved questions.
Key findings
- Mast cells can enhance innate resistance to venoms from 4 species of poisonous snakes, the Gila monster, 2 scorpions, and the honeybee; mast-cell CPA3 detoxifies ET-1/sarafotoxin 6b, and chymase mMCP4 detoxifies VIP/helodermin and Gila monster/scorpion venoms. Human mast cell tryptase also reduced toxicity of venoms from six poisonous snakes in embryonic zebrafish assays.
- Acquired type 2 immune responses to honeybee venom or Russell’s viper venom increase survival against otherwise lethal challenge; resistance was transferable with 250 µL of immune serum, lost after IgE depletion by anti-IgE or heating at 56°C for 1 hour, and absent in IgE-deficient or FcεRI-deficient mice.
- Local IgE plus antigen (DNP-HSA) increased resistance to Russell’s viper venom admixed with DNP-HSA in C57BL/6 and BALB/c mice, whereas anti-DNP IgG1 or IgG2b did not protect and increased early hypothermia.
- Historical guinea pig studies showed anti-basophil serum ablated acquired resistance to *Amblyomma americanum* tick feeding; later mouse studies implicated mast cells, basophils, and IgE in acquired immunity to *Haemaphysalis longicornis*, with basophils possibly more important for *Dermacentor variabilis*.
Methods
- Narrative review, not a primary experimental report; it synthesizes prior studies from the authors and others.
- Evidence base includes mouse genetic models: mast cell-deficient/knock-in mice (WBB6F1-KitW/KitW-v, C57BL/6-KitW-sh/KitW-sh, C57BL/6-Cpa3-Cre+-Mcl-1fl/fl), IgE-deficient and FcεRI-deficient mice, protease-deficient or catalytically inactive CPA3 mice, passive serum transfer, venom challenge, and local IgE sensitization.
- Also cites in vitro embryonic zebrafish assays for human mast cell proteases and historical guinea pig basophil-depletion studies.
Limitations
- Stated: many unresolved questions remain, including whether mechanisms beyond protease release contribute, how venoms induce Th2/IgE responses, the evolutionary importance of ectoparasites/helminths/venomous animals, whether basophils contribute to venom resistance, and why some subjects develop fatal anaphylaxis rather than protection.
- Stated: proving that IgE, mast cells, or basophils dramatically influence survival of parasite-infected animals is challenging; prior parasite studies generally did not analyze overall survival or reproductive success, and some findings suggest effects may favor the parasite.
- Stated/evident: mouse model caveats—each mast cell/basophil deficiency model has features that must be considered, roles may vary by model strength and strain background, and the authors recommend using more than one genetic model; most venom-protection evidence is in mice, with human relevance largely inferential.
Model-written summary. Check it against the paper before relying on it.
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Claims the paper makes
43 Check pending · 26 No full text of the sources · 12 Own interpretation · 6 Not checked yet · 1 Own result
In the paper
“We also found that genetically IgE-deficient mice [97] could not develop acquired immunity to honeybee venom, even though they developed a robust IgG1 antibody response to the venom [96].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > IgE can contribute to host defense against arthropod and reptile venoms.
What the sources say
- Not checked — no full text of the sourcecites [97] Oettgen HC, Martin TR, Wynshaw-Boris A, Deng C, Drazen JM, Leder P. Active anaphylaxis in IgE-deficient mice. Nature. 1994;370:367–70. source
- Check pendingcites [96] Marichal T, Starkl P, Reber LL, Kalesnikoff J, Oettgen HC, Tsai M, et al. A beneficial role for immunoglobulin E in host defense against honeybee venom. Immunity. 2013;39:963–75. source
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In the paper
“Moreover, when such “immune serum” was depleted of IgE (either by adding a neutralizing antibody to IgE [35, 101] or by heating to 56° C for 1 hour, which eliminates the ability of IgE to bind to FcεRI and induce passive cutaneous anaphylaxis [102] while the function of other antibody classes, including IgG1, is not affected [103]), the immune serum’s ability to transfer enhanced resistance to”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > IgE can contribute to host defense against arthropod and reptile venoms.
What the sources say
- Check pendingcites [35] Amiri P, Haak-Frendscho M, Robbins K, McKerrow JH, Stewart T, Jardieu P. Anti-immunoglobulin E treatment decreases worm burden and egg production in schistosoma mansoni-infected normal and interferon gamma knockout mice. J Exp Med. 1994;180:43–51. source
- Check pendingcites [101] Haak-Frendscho M, Saban R, Shields RL, Jardieu PM. Anti-immunoglobulin E antibody treatment blocks histamine release and tissue contraction in sensitized mice. Immunology. 1998;94:115–21. source
- Not checked — no full text of the sourcecites [102] Prouvost-Danon A, Binaghi RA, Abadie A. Effect of heating at 56 degrees C on mouse IgE antibodies. Immunochemistry. 1977;14:81–4. source
- Check pendingcites [103] Strait RT, Morris SC, Finkelman FD. IgG-blocking antibodies inhibit IgE-mediated anaphylaxis in vivo through both antigen interception and FcγRIIb cross-linking. J Clin Invest. 2006;116:833–41. source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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In the paper
“we will describe evidence that mast cells can enhance innate resistance, and survival, to challenge with reptile or arthropod venoms during a first exposure to such venoms.”
- Also stated in: § Identifying a beneficial role for mast cells in enhancing innate resistance to venoms. · hedged
“our initial evidence indicated that mast cells can increase the innate resistance of mice upon their first exposure to the venoms of 3 species of poisonous snakes, the Gila monster, the honeybee, or two especially dangerous scorpions.”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > Abstract
What the sources say
- Not checked — no full text of the sourcecites [15] Metz M, Piliponsky AM, Chen CC, Lammel V, Abrink M, Pejler G, et al. Mast cells can enhance resistance to snake and honeybee venoms. Science. 2006;313:526–30. source
- Check pendingcites [18] Akahoshi M, Song CH, Piliponsky AM, Metz M, Guzzetta A, Abrink M, et al. Mast cell chymase reduces the toxicity of Gila monster venom, scorpion venom, and vasoactive intestinal polypeptide in mice. J Clin Invest. 2011;121:4180–91. source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Identifying a beneficial role for mast cells in enhancing innate resistance to venoms. · hedged
In the paper
“We found that most or all of the acquired resistance induced in mice by a single exposure to honeybee venom was transferable to naïve mice with only 250 microliters of serum from honeybee venom-immunized mice [96].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > IgE can contribute to host defense against arthropod and reptile venoms.
What the sources say
- Not checked yetcites [96] Marichal T, Starkl P, Reber LL, Kalesnikoff J, Oettgen HC, Tsai M, et al. A beneficial role for immunoglobulin E in host defense against honeybee venom. Immunity. 2013;39:963–75. source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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In the paper
“in mice surviving an initial encounter with venom, acquired type 2 immune responses, IgE antibodies, the high affinity IgE receptor (FcεRI), and mast cells can contribute to acquired resistance to the lethal effects of both honeybee venom and Russell’s”
- Also stated in: § Abstract · plain
“high affinity IgE receptor (FcεRI), and mast cells can contribute to acquired resistance to the lethal effects of both honeybee venom and Russell’s viper venom.”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > Abstract
What the sources say
- Check pendingcites [96] Marichal T, Starkl P, Reber LL, Kalesnikoff J, Oettgen HC, Tsai M, et al. A beneficial role for immunoglobulin E in host defense against honeybee venom. Immunity. 2013;39:963–75. source
- Check pendingcites [105] Starkl P, Marichal T, Gaudenzio N, Reber LL, Sibilano R, Tsai M, et al. IgE antibodies, FcεRIα and IgE-mediated local anaphylaxis can limit snake venom toxicity. J Allergy Clin Immunol. 2016;137:246–57. source
plainstates a possible cause- Asserted: passes — The authors put it forward as true.
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- Also stated in: § Abstract · plain
In the paper
“We also showed that “immune serum” from WT mice could passively transfer enhanced resistance to honeybee venom to naïve IgE-deficient mice, unless such “immune serum” was first treated to neutralize IgE or impair its ability to bind to FcεRI [96].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > IgE can contribute to host defense against arthropod and reptile venoms.
What the sources say
- Check pendingcites [96] Marichal T, Starkl P, Reber LL, Kalesnikoff J, Oettgen HC, Tsai M, et al. A beneficial role for immunoglobulin E in host defense against honeybee venom. Immunity. 2013;39:963–75. source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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In the paper
“Finally, we showed that such “immune serum” failed to transfer enhanced venom resistance to mice lacking either the IgE antibody-binding α chain of the FcεRI or the γ chain of FcεRI that is necessary for signaling initiated by aggregation of the receptor [5, 6].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > IgE can contribute to host defense against arthropod and reptile venoms.
What the sources say
- Not checked — no full text of the sourcecites [5] Kinet JP. The high-affinity IgE receptor (Fc epsilon RI): from physiology to pathology. Annu Rev Immunol. 1999;17:931–72. source
- Check pendingcites [6] Rivera J, Fierro NA, Olivera A, Suzuki R. New insights on mast cell activation via the high affinity receptor for IgE. Adv Immunol. 2008;98:85–120. source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Our evidence showed that IgE antibodies were the critical elements of the acquired host resistance to honeybee or Russell’s viper venom.”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > IgE can contribute to host defense against arthropod and reptile venoms.
What the sources say
- Not checked yetcites [96] Marichal T, Starkl P, Reber LL, Kalesnikoff J, Oettgen HC, Tsai M, et al. A beneficial role for immunoglobulin E in host defense against honeybee venom. Immunity. 2013;39:963–75. source
boostedstates a cause- Asserted: passes — The authors put it forward as true.
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In the paper
“We found that, in mice, IgE-associated type 2 immune responses against honeybee venom or Russell’s viper venom were able to increase significantly host resistance to challenge with potentially lethal doses of those venoms [96].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > IgE can contribute to host defense against arthropod and reptile venoms.
What the sources say
- Not checked yetcites [96] Marichal T, Starkl P, Reber LL, Kalesnikoff J, Oettgen HC, Tsai M, et al. A beneficial role for immunoglobulin E in host defense against honeybee venom. Immunity. 2013;39:963–75. source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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In the paper
“However, pre-sensitization of C57BL/6 mice with anti-DNP IgG1 or IgG2b, DNP-specific IgG isotypes with the capacity to activate effector cells via Fcγ receptors [108], not only failed to increase protection but also resulted in increased hypothermia at early time points compared to vehicle-treated or IgE-sensitized mice (Fig 7, B) [105].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > IgE can contribute to host defense against arthropod and reptile venoms.
What the sources say
- Check pendingcites [105] Starkl P, Marichal T, Gaudenzio N, Reber LL, Sibilano R, Tsai M, et al. IgE antibodies, FcεRIα and IgE-mediated local anaphylaxis can limit snake venom toxicity. J Allergy Clin Immunol. 2016;137:246–57. source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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- It may state two separate claims as one. 23
- Probably not a substantial claim. 10
In the paper
“Our initial findings indicate that the propensity to develop protective vs. potentially harmful type 2 immune responses to venoms, at least in mice, can depend on the genetic background of the animal, the type and amount of venom to which the animal is exposed, and/or the frequency of such venom exposures [105].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > Conclusions.
What the sources say
- Check pendingcites [105] Starkl P, Marichal T, Gaudenzio N, Reber LL, Sibilano R, Tsai M, et al. IgE antibodies, FcεRIα and IgE-mediated local anaphylaxis can limit snake venom toxicity. J Allergy Clin Immunol. 2016;137:246–57. source
hedgedstates a possible cause- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Subsequently, we found that the acquired enhanced resistance to Russell’s viper venom (RVV) which we observed in mice that had developed type 2 immune responses to that venom [96] also was highly dependent on IgE (Fig. 5) and FcεRI (see Fig. 4, A–E in ref. [105]), and could be effectively transferred by immune serum into normal mice (see Fig. 3, F–J in ref. [105]) but not into C57BL/6-Cpa3-Cre;Mcl”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > IgE can contribute to host defense against arthropod and reptile venoms.
What the sources say
- Check pendingcites [96] Marichal T, Starkl P, Reber LL, Kalesnikoff J, Oettgen HC, Tsai M, et al. A beneficial role for immunoglobulin E in host defense against honeybee venom. Immunity. 2013;39:963–75. source
- Check pendingcites [105] Starkl P, Marichal T, Gaudenzio N, Reber LL, Sibilano R, Tsai M, et al. IgE antibodies, FcεRIα and IgE-mediated local anaphylaxis can limit snake venom toxicity. J Allergy Clin Immunol. 2016;137:246–57. source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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A check of a cited source is scheduled, or we don’t hold its full text yet; the claim is checked once it runs.
In the paper
“FcεRI are expressed on mast cells, that reside in most vascularized tissues in mammals and other vertebrates, and on basophilic granulocytes (“basophils”), that ordinarily circulate in very low numbers in the blood but which can be recruited to sites of inflammation [3, 5–10].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > Mast cells, basophils and IgE in the pathology of allergic disorders.
What the sources say
- Not checked yetcites [3] Galli SJ, Tsai M. IgE and mast cells in allergic disease. Nat Med. 2012;18:693–704. source
A check is scheduled.
- Not checked — no full text of the sourcecites [5] Kinet JP. The high-affinity IgE receptor (Fc epsilon RI): from physiology to pathology. Annu Rev Immunol. 1999;17:931–72. source
- Check pendingcites [6] Rivera J, Fierro NA, Olivera A, Suzuki R. New insights on mast cell activation via the high affinity receptor for IgE. Adv Immunol. 2008;98:85–120. source
- Check pendingcites [7] Oettgen HC, Geha RS. IgE in asthma and atopy: cellular and molecular connections. J Clin Invest. 1999;104:829–35. source
- Not checked — no full text of the sourcecites [8] Karasuyama H, Mukai K, Obata K, Tsujimura Y, Wada T. Nonredundant roles of basophils in immunity. Annu Rev Immunol. 2011;29:45–69. source
- Check pendingcites [9] Sullivan BM, Liang HE, Bando JK, Wu D, Cheng LE, McKerrow JK, et al. Genetic analysis of basophil function in vivo. Nat Immunol. 2011;12:527–35. source
- Not checked — no full text of the sourcecites [10] Voehringer D. Protective and pathological roles of mast cells and basophils. Nat Rev Immunol. 2013;13:362–75. source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. It may state two separate claims as one.
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In the paper
“Even before Profet’s 1991 paper, James Stebbings, Jr. hypothesized that “a major function of the immediate hypersensitivity reactions has been the protection of terrestrial vertebrates from the bites of, or invasion by, arthropods” [40].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > Possible beneficial functions of mast cells, basophils and IgE.
What the sources say
- Not checked — no full text of the sourcecites [40] Stebbings JH Jr.. Immediate hypersensitivity: a defense against arthropods? Perspect Biol Med. 1974;17:233–9. source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“By undergoing degranulation and releasing proteases that can inactivate potentially toxic endogenous peptides or peptides in venoms, mouse mast cells can help to restore homeostasis, albeit while also enhancing features of the ensuing local and perhaps systemic inflammatory responses.”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > Identifying a beneficial role for mast cells in enhancing innate resistance to venoms.
plainstates a possible cause- Asserted: passes — The authors put it forward as true.
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In the paper
“Such envenomation not only provokes an innate inflammatory response and pathology related to the biological activities of the venoms’ toxins [86–88], but also can induce allergic sensitization associated with the development of specific IgE antibodies [89–94].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > IgE can contribute to host defense against arthropod and reptile venoms.
What the sources say
- Not checked — no full text of the sourcecites [86] Habermann E. Bee and wasp venoms. Science. 1972;177:314–22. source
- Not checked — no full text of the sourcecites [87] Mukherjee AK, Ghosal SK, Maity CR. Some biochemical properties of Russell’s viper (daboia russelli) venom from eastern India: correlation with clinico-pathological manifestation in Russell’s viper bite. Toxicon. 2000;38:163–75. source
- Not checked — no full text of the sourcecites [88] Risch M, Georgieva D, von Bergen M, Jehmlich N, Genov N, Arni RK, et al. Snake venomics of the siamese Russell’s viper (daboia russelli siamensis)—relation to pharmacological activities. J Proteomics. 2009;72:256–69. source
- Not checked — no full text of the sourcecites [89] Saelinger CB, Higginbotham RD. Hypersensitivity responses to bee venom and the mellitin. Int Arch Allergy Appl Immunol. 1974;46:28–37. source
- Not checked — no full text of the sourcecites [90] Charavejasarn CC, Reisman RE, Arbesman CE. Reactions of anti-bee venom mouse reagins and other antibodies with related antigens. Int Arch Allergy Appl Immunol. 1975;48:691–7. source
- Not checked — no full text of the sourcecites [91] Jarisch R, Yman L, Boltz A, Sandor I, Janitsch A. IgE antibodies to bee venom, phospholipase A, melittin and wasp venom. Clin Allergy. 1979;9:535–41. source
- Check pendingcites [92] Wadee AA, Rabson AR. Development of specific IgE antibodies after repeated exposure to snake venom. J Allergy Clin Immunol. 1987;80:695–8. source
- Not checked — no full text of the sourcecites [93] Annila I. Bee venom allergy. Clin Exp Allergy. 2000;30:1682–7. source
- Not checked — no full text of the sourcecites [94] Bilo BM, Rueff F, Mosbech H, Bonifazi F, Oude-Elberink JN. Diagnosis of hymenoptera venom allergy. Allergy. 2005;60:1339–49. source
plainstates an association- Asserted: passes — The authors put it forward as true.
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In the paper
“It was known that when guinea pigs subjected to a single round of exposure to the feeding of larval A. americanum ticks are challenged with a second exposure to the larval ticks about a month later, tick feeding success is markedly diminished, and such acquired resistance can be transferred by administering serum from sensitized to naïve guinea pigs [49].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > Evidence for a beneficial role of basophils in acquired immunity to the feeding of ixodid ticks.
What the sources say
- Not checked — no full text of the sourcecites [49] Brown SJ, Askenase PW. Cutaneous basophil responses and immune resistance of guinea pigs to ticks: passive transfer with peritoneal exudate cells or serum. J Immunol. 1981;127:2163–7. source
boostedstates a cause- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Basophils activated via FcεRI aggregation can release a panel of mediators partially overlapping with those of mast cells, but, as compared to mast cells, they contain much lower amounts of proteases and appear to produce fewer cytokines and chemokines [8–10].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > Mast cells, basophils and IgE in the pathology of allergic disorders.
What the sources say
- Not checked — no full text of the sourcecites [8] Karasuyama H, Mukai K, Obata K, Tsujimura Y, Wada T. Nonredundant roles of basophils in immunity. Annu Rev Immunol. 2011;29:45–69. source
- Check pendingcites [9] Sullivan BM, Liang HE, Bando JK, Wu D, Cheng LE, McKerrow JK, et al. Genetic analysis of basophil function in vivo. Nat Immunol. 2011;12:527–35. source
- Not checked — no full text of the sourcecites [10] Voehringer D. Protective and pathological roles of mast cells and basophils. Nat Rev Immunol. 2013;13:362–75. source
hedged- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A statement the paper makes itself — it cites no source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Mouse mast cells contain at least two different proteases, CPA3 and chymase (mMCP4), which permit such mast cells to respond, after their activation via cognate receptors that can bind either the endogenous or the structurally similar reptile-derived peptides, to high and potentially toxic levels of ET-1 and VIP, respectively.”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > Identifying a beneficial role for mast cells in enhancing innate resistance to venoms.
plainstates a cause- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Profet proposed that acute allergic reactions, manifested as immediately occurring symptoms in response to allergen exposure, such as sneezing, coughing, vomiting and diarrhea, evolved as defense mechanisms allowing the sensitized host to respond immediately to, and to expel, neutralize and/or avoid, noxious substances which might be indicative of potentially life-threatening situations [39].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > Possible beneficial functions of mast cells, basophils and IgE.
What the sources say
- Not checked — no full text of the sourcecites [39] Profet M. The function of allergy: immunological defense against toxins. Q Rev Biol. 1991;66:23–62. source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Early work by Higginbotham and colleagues suggested that mast cells might be able to diminish the toxicity of certain venoms by degranulating and releasing heparin in response to venom exposure [76, 77].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > Identifying a beneficial role for mast cells in enhancing innate resistance to venoms.
What the sources say
- Not checked — no full text of the sourcecites [76] Higginbotham RD. Mast cells and local resistance to Russell’s viper venom. J Immunol. 1965;95:867–75. source
- Not checked — no full text of the sourcecites [77] Higginbotham RD, Karnella S. The significance of the mast cell response to bee venom. J Immunol. 1971;106:233–40. source
hedgedstates a possible cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“However, the recipient W/Wv mice also were cured of their anemia [56], as was initially shown by Elizabeth Russell [57].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > “Mast cell knock-in mice”.
What the sources say
- Not checked — no full text of the sourcecites [56] Kitamura Y, Go S, Hatanaka K. Decrease of mast cells in W/Wv mice and their increase by bone marrow transplantation. Blood. 1978;52:447–52. source
- Not checked — no full text of the sourcecites [57] Russell ES. Hereditary anemias of the mouse: a review for geneticists. Adv Genet. 1979;20:357–459. source
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Hiroshi Matsuda and Yukihiko Kitamura and colleagues (using mast cell-engrafted genetically mast cell deficient (WB/Re-W/+ X C57BL/6-Wv/+)F1-”W/Wv” mice) [51], and Hajime Karasuyama and colleagues (using mice genetically deficient in basophils [52]), provided evidence that both mast cells and basophils, as well as IgE, can contribute to acquired immunity to the feeding of Haemaphysalis longicornis”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > Evidence for a beneficial role of basophils in acquired immunity to the feeding of ixodid ticks.
What the sources say
- Not checked — no full text of the sourcecites [51] Matsuda H, Watanabe N, Kiso Y, Hirota S, Ushio H, Kannan Y, et al. Necessity of IgE antibodies and mast cells for manifestation of resistance against larval haemaphysalis longicornis ticks in mice. J Immunol. 1990;144:259–62. source
- Check pendingcites [52] Wada T, Ishiwata K, Koseki H, Ishikura T, Ugajin T, Ohnuma N, et al. Selective ablation of basophils in mice reveals their nonredundant role in acquired immunity against ticks. J Clin Invest. 2010;120:2867–75. source
plainstates a possible cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Treatment with rabbit AES had a lesser, but still statistically significant, effect on tick feeding success, whereas normal rabbit serum was without effect (Fig. 1) [45].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > Evidence for a beneficial role of basophils in acquired immunity to the feeding of ixodid ticks.
What the sources say
- Not checked — no full text of the sourcecites [45] Brown SJ, Galli SJ, Gleich GJ, Askenase PW. Ablation of immunity to amblyomma americanum by anti-basophil serum: cooperation between basophils and eosinophils in expression of immunity to ectoparasites (ticks) in guinea pigs. J Immunol. 1982;129:790–6. source
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“We recently showed that this approach also can be pursued using C57BL/6-Cpa3-Cre+-Mcl-1fl/fl mice, which are mast cell-deficient (and also have substantially diminished numbers and function of basophils) due to the lineage-restricted ablation of the anti-apoptotic factor, myeloid cell leukemia 1 (Mcl-1), in lineages with sufficiently high expression of the Cpa3 gene [70].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > “Mast cell knock-in mice”.
What the sources say
- Check pendingcites [70] Lilla JN, Chen CC, Mukai K, BenBarak MJ, Franco CB, Kalesnikoff J, et al. Reduced mast cell and basophil numbers and function in Cpa3-Cre; Mcl‑1fl/fl mice. Blood. 2011;118:6930–8. source
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“ABS did cause a reduction in skin mast cell numbers if injected intra-dermally, raising the possibility that the antiserum targeted an antigen shared by basophils and mast cells.”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > Evidence for a beneficial role of basophils in acquired immunity to the feeding of ixodid ticks.
What the sources say
- Not checked — no full text of the sourcecites [43] Galli SJ, Colvin RB, Verderber E, Galli AS, Monahan R, Dvorak AM, et al. Preparation of a rabbit anti-guinea pig basophil serum: in vitro and in vivo characterization. J Immunol. 1978;121:1157–66. source
hedgedstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“For example, certain peptides such as substance P can activate some mast cell populations to robustly release the granule-stored mediators; however, compared to the same cells activated via the FcεRI, such stimuli may less potently elicit release of lipid mediators or cytokines [14, 20, 21].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > Innate activation of mast cells.
What the sources say
- Not checked — no full text of the sourcecites [14] Galli SJ, Kalesnikoff J, Grimbaldeston MA, Piliponsky AM, Williams CM, Tsai M. Mast cells as “tunable” effector and immunoregulatory cells: recent advances. Annu Rev Immunol. 2005;23:749–86. source
- Not checked — no full text of the sourcecites [20] Jensen BM, Frandsen PM, Raaby EM, Schiotz PO, Skov PS, Poulsen LK. Molecular and stimulus-response profiles illustrate heterogeneity between peripheral and cord blood-derived human mast cells. J Leukoc Biol. 2014;95:893–901. source
- Check pendingcites [21] McNeil BD, Pundir P, Meeker S, Han L, Undem BJ, Kulka M, et al. Identification of a mast-cell-specific receptor crucial for pseudo-allergic drug reactions. Nature. 2015;519:237–41. source
hedgedstates a possible cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Yukihiko Kitamura and colleagues discovered that (WB/Re-W/+ X C57BL/6-Wv/+)F1-”W/Wv” mice (now known as WBB6F1-KitW/KitW-v mice, since “W” later was shown to encode c-kit [54, 55]) not only had a moderate macrocytic anemia, a phenotype which had been reported decades earlier, but were profoundly deficient in tissue mast cells [56].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > “Mast cell knock-in mice”.
What the sources say
- Not checked — no full text of the sourcecites [54] Chabot B, Stephenson DA, Chapman VM, Besmer P, Bernstein A. The proto-oncogene c‑kit encoding a transmembrane tyrosine kinase receptor maps to the mouse W locus. Nature. 1988;335:88–9. source
- Not checked — no full text of the sourcecites [55] Geissler EN, Ryan MA, Housman DE. The dominant-white spotting (W) locus of the mouse encodes the c‑kit proto-oncogene. Cell. 1988;55:185–92. source
- Not checked — no full text of the sourcecites [56] Kitamura Y, Go S, Hatanaka K. Decrease of mast cells in W/Wv mice and their increase by bone marrow transplantation. Blood. 1978;52:447–52. source
plainstates an association- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Brown et al. found that treatment of tick-sensitized guinea pigs with rabbit ABS markedly diminished basophils in the bone marrow, blood, and skin at sites of tick feeding of the sensitized guinea pigs, and also resulted in diminished numbers of eosinophils at such feeding sites [45].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > Evidence for a beneficial role of basophils in acquired immunity to the feeding of ixodid ticks.
What the sources say
- Not checked — no full text of the sourcecites [45] Brown SJ, Galli SJ, Gleich GJ, Askenase PW. Ablation of immunity to amblyomma americanum by anti-basophil serum: cooperation between basophils and eosinophils in expression of immunity to ectoparasites (ticks) in guinea pigs. J Immunol. 1982;129:790–6. source
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Nakano et al. showed that the transfer of WBB6F1-+/+ mouse bone marrow-derived cultured mast cells (BMCMCs) i.v., i.p. or i.d. into WBB6F1-W/Wv mice had no effect on the anemia of the recipient mice but resulted in the appearance of mast cells in their tissues, and that, over time, these mast cell populations came to exhibit certain phenotypic features similar to those present in the corresponding”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > “Mast cell knock-in mice”.
What the sources say
- Check pendingcites [63] Nakano T, Sonoda T, Hayashi C, Yamatodani A, Kanayama Y, Yamamura T, et al. Fate of bone marrow-derived cultured mast cells after intracutaneous, intraperitoneal, and intravenous transfer into genetically mast cell-deficient W/Wv mice. Evidence that cultured mast cells can give rise to both connective tissue type and mucosal mast cells. J Exp Med. 1985;162:1025–43. source
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“This work showed that mast cells could diminish the toxicity of VIP, helodermin, and the whole venom of H. suspectum, and that this was largely or wholly dependent on mast cell-derived mMCP4 rather than CPA3 [18].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > Identifying a beneficial role for mast cells in enhancing innate resistance to venoms.
What the sources say
- Not checked yetcites [18] Akahoshi M, Song CH, Piliponsky AM, Metz M, Guzzetta A, Abrink M, et al. Mast cell chymase reduces the toxicity of Gila monster venom, scorpion venom, and vasoactive intestinal polypeptide in mice. J Clin Invest. 2011;121:4180–91. source
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Abnormalities in host responses to certain parasites have been observed in mice that genetically lack IgE [27, 28], mast cells [29–33], or basophils [28, 33] but such studies generally have not included an analysis of the effects of those deficiencies on the overall survival or reproductive success of the infected hosts.”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > Possible beneficial functions of mast cells, basophils and IgE.
What the sources say
- Not checked — no full text of the sourcecites [27] Spencer LA, Porte P, Zetoff C, Rajan TV. Mice genetically deficient in immunoglobulin E are more permissive hosts than wild-type mice to a primary, but not secondary, infection with the filarial nematode Brugia malayi. Infect Immun. 2003;71:2462–7. source
- Check pendingcites [28] Schwartz C, Turqueti-Neves A, Hartmann S, Yu P, Nimmerjahn F, Voehringer D. Basophil-mediated protection against gastrointestinal helminths requires IgE-induced cytokine secretion. Proc Natl Acad Sci USA. 2014;111:E5169–77. source
- Not checked — no full text of the sourcecites [29] Nawa Y, Kiyota M, Korenaga M, Kotani M. Defective protective capacity of W/Wv mice against strongyloides ratti infection and its reconstitution with bone marrow cells. Parasite Immunol. 1985;7:429–38. source
- Check pendingcites [30] Knight PA, Wright SH, Lawrence CE, Paterson YY, Miller HR. Delayed expulsion of the nematode trichinella spiralis in mice lacking the mucosal mast cell-specific granule chymase, mouse mast cell protease‑1. J Exp Med. 2000;192:1849–56. source
- Check pendingcites [31] Furuta T, Kikuchi T, Iwakura Y, Watanabe N. Protective roles of mast cells and mast cell-derived TNF in murine malaria. J Immunol. 2006;177:3294–302. source
- Not checked — no full text of the sourcecites [32] Maurer M, Lopez Kostka S, Siebenhaar F, Moelle K, Metz M, Knop J, et al. Skin mast cells control T cell-dependent host defense in Leishmania major infections. FASEB J. 2006;20:2460–7. source
- Not checked — no full text of the sourcecites [33] Ohnmacht C, Voehringer D. Basophils protect against reinfection with hookworms independently of mast cells and memory Th2 cells. J Immunol. 2010;184:344–50. source
plainstates an association- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These findings support the hypothesis that mast cells and IgE can help protect the host against venoms and perhaps other noxious substances.”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > Abstract
plainstates a possible cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Metz et al. showed that mast cells not only diminished the toxicity of sarafotoxin 6b and enhanced the survival of mice injected with that peptide, but also did so in mice injected with the whole venom of A. engaddensis [15].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > Identifying a beneficial role for mast cells in enhancing innate resistance to venoms.
What the sources say
- Not checked — no full text of the sourcecites [15] Metz M, Piliponsky AM, Chen CC, Lammel V, Abrink M, Pejler G, et al. Mast cells can enhance resistance to snake and honeybee venoms. Science. 2006;313:526–30. source
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“When mast cell- or basophil-bound IgE antibodies recognize antigens that are at least bivalent, rapid aggregation of the FcεRI initiates complex intra-cellular signaling pathways. This ultimately results in the release, by such activated effector cells, of a wide variety of mediators with diverse biological effects [5, 6, 8–11].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > Mast cells, basophils and IgE in the pathology of allergic disorders.
What the sources say
- Not checked — no full text of the sourcecites [5] Kinet JP. The high-affinity IgE receptor (Fc epsilon RI): from physiology to pathology. Annu Rev Immunol. 1999;17:931–72. source
- Check pendingcites [6] Rivera J, Fierro NA, Olivera A, Suzuki R. New insights on mast cell activation via the high affinity receptor for IgE. Adv Immunol. 2008;98:85–120. source
- Not checked — no full text of the sourcecites [8] Karasuyama H, Mukai K, Obata K, Tsujimura Y, Wada T. Nonredundant roles of basophils in immunity. Annu Rev Immunol. 2011;29:45–69. source
- Check pendingcites [9] Sullivan BM, Liang HE, Bando JK, Wu D, Cheng LE, McKerrow JK, et al. Genetic analysis of basophil function in vivo. Nat Immunol. 2011;12:527–35. source
- Not checked — no full text of the sourcecites [10] Voehringer D. Protective and pathological roles of mast cells and basophils. Nat Rev Immunol. 2013;13:362–75. source
- Check pendingcites [11] Kawakami T, Kitaura J. Mast cell survival and activation by IgE in the absence of antigen: a consideration of the biologic mechanisms and relevance. J Immunol. 2005;175:4167–73. source
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“In addition to using the original mast cell-deficient WBB6F1-KitW/KitW-v mice to prepare “mast cell knock-in mice”, this approach also can be employed using C57BL/6-KitW-sh/KitW-sh mice, which have the advantage of being inbred, fertile and not anemic [68, 69, 73].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > “Mast cell knock-in mice”.
What the sources say
- Check pendingcites [68] Grimbaldeston MA, Chen CC, Piliponsky AM, Tsai M, Tam SY, Galli SJ. Mast cell-deficient W‑sash c‑kit mutant KitW‑sh/W-sh mice as a model for investigating mast cell biology in vivo. Am J Pathol. 2005;167:835–48. source
- Check pendingcites [69] Wolters PJ, Mallen-St. Clair J, Lewis CC, Villalta SA, Baluk P, Erle DJ, et al. Tissue-selective mast cell reconstitution and differential lung gene expression in mast cell-deficient KitW‑sh/KitW‑sh sash mice. Clin Exp Allergy. 2005;35:82–8. source
- Check pendingcites [73] Nigrovic PA, Gray DH, Jones T, Hallgren J, Kuo FC, Chaletzky B, et al. Genetic inversion in mast cell-deficient Wsh mice interrupts corin and manifests as hematopoietic and cardiac aberrancy. Am J Pathol. 2008;173:1693–701. source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Such tunicates also have been reported to have cells resembling basophils [111].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > Conclusions.
What the sources say
- Not checked — no full text of the sourcecites [111] de Barros CM, Andrade LR, Allodi S, Viskov C, Mourier PA, Cavalcante MC, et al. The Hemolymph of the ascidian styela plicata (chordata-tunicata) contains heparin inside basophil-like cells and a unique sulfated galactoglucan in the plasma. J Biol Chem. 2007;282:1615–26. source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Independently of our work, Palm et al. showed that mice immunized with the major allergen contained in honeybee venom, bee venom phospholipase A2 (bvPLA2), exhibited enhanced resistance to the ability of bvPLA2 to induce hypothermia upon its injection into mice, and also provided evidence that this enhanced immunity required B cells and was diminished significantly in mice which lacked the IgE”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > IgE can contribute to host defense against arthropod and reptile venoms.
What the sources say
- Check pendingcites [104] Palm NW, Rosenstein RK, Yu S, Schenten DD, Florsheim E, Medzhitov R. Bee venom phospholipase A2 induces a primary type 2 response that is dependent on the receptor ST2 and confers protective immunity. Immunity. 2013;39:976–85. source
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“DNP-specific IgG isotypes with the capacity to activate effector cells via Fcγ receptors [108]”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > IgE can contribute to host defense against arthropod and reptile venoms.
What the sources say
- Not checked — no full text of the sourcecites [108] Bruhns P. Properties of mouse and human IgG receptors and their contribution to disease models. Blood. 2012;119:5640–9. source
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
In the paper
“The latter finding suggested that mast cells can contribute to IgE-mediated acquired resistance to honeybee venom, as well as enhance the innate resistance of mice to a first exposure to that venom [15].”
§ Mast cells and IgE in defense against lethality of venoms: Possible “benefit” of allergy[1] > IgE can contribute to host defense against arthropod and reptile venoms.
What the sources say
- Not checked — no full text of the sourcecites [15] Metz M, Piliponsky AM, Chen CC, Lammel V, Abrink M, Pejler G, et al. Mast cells can enhance resistance to snake and honeybee venoms. Science. 2006;313:526–30. source
hedgedstates a possible cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
Findings in mice about mast cells, IgE, and venom resistance are relevant to human allergy and venom defense.
“These findings support the hypothesis that mast cells and IgE can help protect the host against venoms and perhaps other noxious substances.”
The paper relies on this without support.
The venoms used in mouse experiments are representative of animal venoms that threaten humans.
“our initial evidence indicated that mast cells can increase the innate resistance of mice upon their first exposure to the venoms of 3 species of poisonous snakes, the Gila monster, the honeybee, or two especially dangerous scorpions.”
The paper relies on this without support.
Vertebrates have been subjected to evolutionary pressure through millions of years of co-evolution with venomous arthropods, reptiles, and other species.
“However, in addition to parasites, vertebrates also have been subjected to evolutionary pressure through millions of years of co-evolution with venomous arthropods, reptiles, and other species.”
Citations
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IgE and mast cells in allergic disease
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The dominant-white spotting (W) locus of the mouse encodes the c-kit proto-oncogene
Geissler, E. N., Ryan, M. A., & Housman, D. E. (1988) · Cell · doi:10.1016/0092-8674(88)90020-7 · Cited by 1,287
Identification of a mast-cell-specific receptor crucial for pseudo-allergic drug reactions
McNeil, B. D., Pundir, P., Meeker, S., Han, L., Undem, B. J., Kulka, M., & Dong, X. (2015) · Nature · doi:10.1038/nature14022 · Cited by 1,228
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Self-citationMAST CELLS AS “TUNABLE” EFFECTOR AND IMMUNOREGULATORY CELLS: Recent Advances
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The proto-oncogene c-kit encoding a transmembrane tyrosine kinase receptor maps to the mouse W locus
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THE HIGH-AFFINITY I g E RECEPTOR (FcεRI): From Physiology to Pathology
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Research works printed but not linked: 1
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Cellular and molecular mechanisms of allergic asthma
Komlósi, Z. I., van de Veen, W., Kovács, N., Szűcs, G., Sokołowska, M., O’Mahony, L., Akdiş, M., & Akdiş, C. A. (2021) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2021.100995 · Cited by 271
Landscape of mast cell populations across organs in mice and humans
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Metadata
- Authors
- Galli, S. J., Metz, M., Starkl, P., Marichal, T., & Tsai, M.
- Affiliations
- Stanford Medicine (US)
- Charité – Universitätsmedizin Berlin (DE)
- Austrian Academy of Sciences (AT)
- University of Liège (BE)
- Corresponding author
- Galli, Stephen J.
- Venue
- Allergo Journal International
- Published
- 2020-03
- Volume
- 29
- Issue
- 2
- Pages
- 46-62
- ISSN
- 2197-0378 (ISSN-L)
- PMC
- PMC7673288
- OpenAlex
- W3009230457
- Cited by
- 57
- References
- 116
- Citations by year
- 2026: 13 · 2025: 14 · 2024: 6 · 2023: 6 · 2022: 8 · 2021: 9 · 2020: 1
- FWCI
- 2.05
- Type
- journal article
- Language
- en
- Open access
- green
- pmc.ncbi.nlm.nih.gov
- Locations
- Allergo Journal International (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- ORBi (University of Liège) (submittedVersion)
- Funders
- National Cancer Institute (R01CA072074)
- National Institute of Allergy and Infectious Diseases (R01AI023990, R37AI023990, U19AI104209)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR067145)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Mast cells and histamine
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Toxicology › Venomous Animal Envenomation and Studies
- Health Sciences › Medicine › Immunology and Allergy › Food Allergy and Anaphylaxis Research
- Keywords
- mast cells, IgE, venom resistance, anaphylaxis, Th2 immune response, FcεRI, basophils, honey bee venom, Russell's viper venom, helminth immunity, tick immunity, adaptive immunity, innate immunity, allergy
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