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The ingenious mast cell: Contemporary insights into mast cell behavior and function

Dahlin, Joakim S., Maurer, Marcus, Metcalfe, Dean D., Pejler, Gunnar, Sagi‐Eisenberg, Ronit, Nilsson, Gunnar·2022·Allergy
DOI 10.1111/all.14881
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Abstract

Mast cells are (in)famous for their role in allergic diseases, but the physiological and pathophysiological roles of this ingenious cell are still not fully understood. Mast cells are important for homeostasis and surveillance of the human system, recognizing both endogenous and exogenous agents, which induce release of a variety of mediators acting on both immune and non‐immune cells, including nerve cells, fibroblasts, endothelial cells, smooth muscle cells, and epithelial cells. During recent years, clinical and experimental studies on human mast cells, as well as experiments using animal models, have resulted in many discoveries that help decipher the function of mast cells in health and disease. In this review, we focus particularly on new insights into mast cell biology, with a focus on mast cell development, recruitment, heterogeneity, and reactivity. We also highlight the development in our understanding of mast cell‐driven diseases and discuss the development of novel strategies to treat such conditions.

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Image 1
CC-BY-NC-ND · From the PDF
FIGURE 1 Mast cell activation pathways and release of mediators. Mast cells are endowed with a palette of receptors that can recognize endogenous and exogenous products and release different sets of mediators dependent on the receptor involved. Upon recognition mast cells react by releasing mediators through one or several pathways: (1) degranulation and release of granules containing, for example, histamine, heparin, proteases, and cytokines; (2) release of newly synthesized lipid mediators such as PGD 2 , LTC 4 /D 4 /E 4 , TXA 2 and 15-­ HETE; (3) release of de novo-­ synthesized cytokines, chemokines, growth factors, and interferons; (4) release of extracellular vesicles, for example, exosomes, containing proteins, mRNA and miRNA
FIGURE 1 Mast cell activation pathways and release of mediators. Mast cells are endowed with a palette of receptors that can recognize endogenous and exogenous products and release different sets of mediators dependent on the receptor involved. Upon recognition mast cells react by releasing mediators through one or several pathways: (1) degranulation and release of granules containing, for example, histamine, heparin, proteases, and cytokines; (2) release of newly synthesized lipid mediators such as PGD 2 , LTC 4 /D 4 /E 4 , TXA 2 and 15-­ HETE; (3) release of de novo-­ synthesized cytokines, chemokines, growth factors, and interferons; (4) release of extracellular vesicles, for example, exosomes, containing proteins, mRNA and miRNACC-BY-NC-ND · From the PDF
FIGURE 2 Differential release of mediators. Depending on ligand -­ receptor interaction mast cells react by releasing different sets of mediators, those stored in granules, newly synthesized and secreted lipid mediators, and de novo produced proteins. Mast cells activated with allergen binding to IgE bound to the high-­ affinity IgE receptor, Fc ε RI, induces degranulation, secretion of lipid mediators and different types of proteins, including cytokines and chemokines. In contrast, the alarmin IL-­ 33 does not induce degranulation but causes secretion of lipid mediators, cytokines and chemokines. 185 The costimulatory molecule CD30 induces secretion of only cytokines and chemokines. 23 Viral infection leads to a variety of responses, depending on the type of virus encountered. 15 For example, respiratory syncytial virus infection induces production of type I interferons and chemokines 24
FIGURE 2 Differential release of mediators. Depending on ligand -­ receptor interaction mast cells react by releasing different sets of mediators, those stored in granules, newly synthesized and secreted lipid mediators, and de novo produced proteins. Mast cells activated with allergen binding to IgE bound to the high-­ affinity IgE receptor, Fc ε RI, induces degranulation, secretion of lipid mediators and different types of proteins, including cytokines and chemokines. In contrast, the alarmin IL-­ 33 does not induce degranulation but causes secretion of lipid mediators, cytokines and chemokines. 185 The costimulatory molecule CD30 induces secretion of only cytokines and chemokines. 23 Viral infection leads to a variety of responses, depending on the type of virus encountered. 15 For example, respiratory syncytial virus infection induces production of type I interferons and chemokines 24CC-BY-NC-ND · From the PDF
Image 4
CC-BY-NC-ND · From the PDF
Image 5
CC-BY-NC-ND · From the PDF
FIGURE 4 Models representing mast cell differentiation in hematopoiesis. (A) The tree-­ like model represents hematopoiesis as a strict series of branching events, in which cell lineage potential is lost at defined checkpoints along with differentiation from hematopoietic stem cells to lineage-­ committed cells. The position of the mast cell branch in this model is controversial. (B) The hematopoietic landscape model represents a continuum of single differentiating progenitors, in which there are multiple paths from hematopoietic stem cells to each lineage's entry point. Ba, basophil; Eo, eosinophil; Ery, erythrocyte, Gr, granulocyte(which commonly refers to basophils, eosinophils, and neutrophils), HSC, hematopoietic stem cell; Ly, lymphocyte; MC, mast cell; MK, megakaryocyte; Mo, monocyte, Neu, neutrophil
FIGURE 4 Models representing mast cell differentiation in hematopoiesis. (A) The tree-­ like model represents hematopoiesis as a strict series of branching events, in which cell lineage potential is lost at defined checkpoints along with differentiation from hematopoietic stem cells to lineage-­ committed cells. The position of the mast cell branch in this model is controversial. (B) The hematopoietic landscape model represents a continuum of single differentiating progenitors, in which there are multiple paths from hematopoietic stem cells to each lineage's entry point. Ba, basophil; Eo, eosinophil; Ery, erythrocyte, Gr, granulocyte(which commonly refers to basophils, eosinophils, and neutrophils), HSC, hematopoietic stem cell; Ly, lymphocyte; MC, mast cell; MK, megakaryocyte; Mo, monocyte, Neu, neutrophilCC-BY-NC-ND · From the PDF
Image 7
CC-BY-NC-ND · From the PDF
FIGURE 5 Fate decisions in the life of the mast cell. Mast cell progenitors (MCp) in the bone marrow (1) are entering the bloodstream and are recruited into the tissue (2). During this process, the cells have to avoid premature degranulation (2). In the tissue (3) MCs can degranulate in three possible modes, either by full exocytosis, compound exocytosis, or by kiss-­ and-­ run exocytosis
FIGURE 5 Fate decisions in the life of the mast cell. Mast cell progenitors (MCp) in the bone marrow (1) are entering the bloodstream and are recruited into the tissue (2). During this process, the cells have to avoid premature degranulation (2). In the tissue (3) MCs can degranulate in three possible modes, either by full exocytosis, compound exocytosis, or by kiss-­ and-­ run exocytosisCC-BY-NC-ND · From the PDF
Image 9
CC-BY-NC-ND · From the PDF
Image 10
CC-BY-NC-ND · From the PDF
FIGURE 6 MC-­ targeted treatments under development. Examples of treatments currently under development that target mast cell mediators, receptors, or their signaling molecules
FIGURE 6 MC-­ targeted treatments under development. Examples of treatments currently under development that target mast cell mediators, receptors, or their signaling moleculesCC-BY-NC-ND · From the PDF
Image 12
CC-BY-NC-ND · From the PDF
Image 13
CC-BY-NC-ND · From the PDF
Image 14
CC-BY-NC-ND · From the PDF
FIGURE 7 Intracellular targets to inhibit MC-­ activating receptors Fc ε RI and KIT. Small molecular inhibitors that target Syk or BTK downstream of Fc ε RI inhibit the downstream signaling. The KIT-­ inhibitors target the kinase activity of the receptor. Imatinib and Nilotinib target only wild-­ type KIT, while Midostaurin and Avapritinib also target D816V-­ mutated KIT that is commonly found in systemic mastocytosis
FIGURE 7 Intracellular targets to inhibit MC-­ activating receptors Fc ε RI and KIT. Small molecular inhibitors that target Syk or BTK downstream of Fc ε RI inhibit the downstream signaling. The KIT-­ inhibitors target the kinase activity of the receptor. Imatinib and Nilotinib target only wild-­ type KIT, while Midostaurin and Avapritinib also target D816V-­ mutated KIT that is commonly found in systemic mastocytosisCC-BY-NC-ND · From the PDF
Image 16
CC-BY-NC-ND · From the PDF
Image 17
CC-BY-NC-ND · From the PDF

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Research works printed but not linked: 174

  1. 10.1182/blood-2017-03-773374 · DOI
  2. 10.1016/j.jaci.2018.01.034 · DOI
  3. 10.1038/nature14022 · DOI · Paper page
  4. 10.18176/jiaci.0557 · DOI
  5. 10.1016/j.jaci.2016.04.051 · DOI
  6. 10.1016/j.jaci.2020.08.027 · DOI
  7. 10.1016/j.neuron.2019.01.012 · DOI
  8. 10.1016/j.immuni.2019.03.013 · DOI
  9. 10.3389/fimmu.2020.559589 · DOI
  10. 10.1038/s41590-019-0493-z · DOI
  11. 10.3389/fimmu.2012.00082 · DOI
  12. 10.1111/all.12004 · DOI
  13. 10.1016/j.jid.2019.01.013 · DOI
  14. 10.3389/fimmu.2019.01361 · DOI
  15. 10.3390/ijms20174241 · DOI
  16. 10.1038/nri3690 · DOI · Paper page
  17. 10.1111/j.1600-065X.2007.00512.x · DOI
  18. 10.1016/j.ejphar.2015.02.058 · DOI
  19. 10.1111/imr.12634 · DOI
  20. 10.3389/fimmu.2014.00569 · DOI
  21. 10.4049/jimmunol.1003383 · DOI
  22. 10.1016/j.jaci.2018.06.033 · DOI
  23. 10.1172/JCI24274 · DOI
  24. 10.1016/j.jaci.2015.01.042 · DOI
  25. 10.1111/j.1600-065X.2007.00519.x · DOI
  26. 10.1016/j.jaci.2021.01.002 · DOI
  27. 10.4049/jimmunol.166.2.868 · DOI
  28. 10.1038/ncb1596 · DOI · Paper page
  29. 10.3390/ijms21155464 · DOI
  30. 10.1073/pnas.1809938115 · DOI
  31. 10.1016/j.it.2017.10.005 · DOI
  32. 10.1111/all.13657 · DOI
  33. 10.1146/annurev-immunol-071719-094903 · DOI
  34. 10.1016/j.it.2020.06.006 · DOI
  35. 10.3390/ijms20184397 · DOI
  36. 10.1016/j.trsl.2016.01.005 · DOI
  37. 10.3390/ijms20122851 · DOI
  38. 10.1111/exd.13907 · DOI
  39. 10.1016/j.coi.2020.05.003 · DOI
  40. 10.1038/nature01320 · DOI · Paper page
  41. 10.1016/j.jaci.2018.10.054 · DOI
  42. 10.1016/0012-1606(83)90066-0 · DOI · Paper page
  43. 10.1016/j.immuni.2018.09.023 · DOI · Paper page
  44. 10.1016/j.immuni.2018.04.025 · DOI · Paper page
  45. 10.1111/all.13668 · DOI · Paper page
  46. 10.1038/268442a0 · DOI
  47. 10.1016/j.jid.2020.03.963 · DOI · Paper page
  48. 10.1182/blood.V94.7.2333.419k30_2333_2342 · DOI
  49. 10.1073/pnas.0509148102 · DOI · Paper page
  50. 10.1016/j.stem.2010.02.013 · DOI
  51. 10.1016/j.stemcr.2020.06.008 · DOI
  52. 10.1371/journal.ppat.1008579 · DOI
  53. 10.1073/pnas.0504197102 · DOI · Paper page
  54. 10.1182/blood-2013-02-483792 · DOI
  55. 10.1182/bloodadvances.2018019539 · DOI · Paper page
  56. 10.1038/nature25022 · DOI
  57. 10.1182/blood-2017-12-821413 · DOI · Paper page
  58. 10.1111/all.14633 · DOI
  59. 10.1016/j.immuni.2013.06.012 · DOI
  60. 10.1111/all.13981 · DOI
  61. 10.1126/sciimmunol.aau7148 · DOI
  62. 10.1038/s41586-020-2316-7 · DOI
  63. 10.1016/j.jaci.2005.02.030 · DOI
  64. 10.1182/blood.V80.12.3009.3009 · DOI
  65. 10.1111/apm.1966.66.3.289 · DOI
  66. Enerbäck L, 1966, Mast cells in rat gastrointestinal mucosa. II. Dye‐binding and metachromatic properties, Acta Pathol Microbiol Scand, 66, 302
  67. 10.1073/pnas.83.12.4464 · DOI
  68. 10.1111/1523-1747.ep12468966 · DOI
  69. 10.1016/0091-6749(88)90199-6 · DOI
  70. 10.1038/mi.2014.91 · DOI · Paper page
  71. 10.1084/jem.20200321 · DOI · Paper page
  72. 10.1126/sciimmunol.abb7221 · DOI · Paper page
  73. 10.1136/thx.2008.101683 · DOI
  74. 10.1164/rccm.200906-0932OC · DOI · Paper page
  75. 10.1016/j.jaci.2013.02.011 · DOI
  76. 10.1038/ni.3445 · DOI
  77. 10.1016/j.immuni.2020.01.012 · DOI
  78. 10.1182/blood-2015-06-650648 · DOI
  79. 10.1084/jem.194.9.1243 · DOI · Paper page
  80. 10.1007/978-1-4419-9533-9_2 · DOI
  81. 10.3389/fimmu.2020.00321 · DOI
  82. 10.1159/000087640 · DOI
  83. 10.3389/fimmu.2012.00119 · DOI
  84. 10.1182/blood.V93.9.2791 · DOI
  85. 10.1002/1521-4141(200012)30:12<3614::AID-IMMU3614>3.0.CO;2-B · DOI
  86. 10.1016/S0006-291X(02)02244-1 · DOI
  87. Taub D, 1995, Bone marrow‐derived murine mast cells migrate, but do not degranulate, in response to chemokines, J Immunol, 154, 2393, 10.4049/jimmunol.154.5.2393 · DOI
  88. 10.1002/eji.1830230329 · DOI
  89. 10.1074/jbc.M408725200 · DOI
  90. 10.4049/jimmunol.169.8.4586 · DOI
  91. 10.1016/j.jaci.2019.06.028 · DOI
  92. 10.1111/j.1600-0854.2005.00372.x · DOI
  93. 10.1172/JCI85538 · DOI
  94. 10.1369/jhc.5R6647.2005 · DOI
  95. 10.1186/1756-0500-4-322 · DOI
  96. 10.1038/s41598-018-23620-y · DOI
  97. 10.1080/1042819021000047001 · DOI
  98. 10.1038/297229a0 · DOI
  99. 10.1016/0006-2952(85)90675-6 · DOI
  100. 10.1074/jbc.M412126200 · DOI
  101. 10.4049/jimmunol.1302196 · DOI
  102. 10.1038/s41598-017-15047-8 · DOI
  103. 10.3389/fimmu.2014.00453 · DOI
  104. 10.1016/j.semcdb.2017.02.002 · DOI
  105. 10.1158/0008-5472.CAN-16-2234 · DOI
  106. Metcalfe DD, 2019, Wintrobe’s Clinical Hematology, 1793
  107. 10.1056/NEJMoa1500611 · DOI
  108. 10.1111/all.14065 · DOI
  109. 10.1016/j.jaci.2014.03.007 · DOI
  110. 10.1159/000359963 · DOI
  111. 10.1007/164_2016_130 · DOI
  112. 10.1016/j.cell.2019.09.009 · DOI
  113. 10.1183/13993003.00685-2019 · DOI
  114. 10.3389/fimmu.2018.00689 · DOI
  115. 10.1159/000507218 · DOI
  116. 10.1111/all.14412 · DOI
  117. 10.1056/NEJMoa1215372 · DOI
  118. 10.1056/NEJMoa1900408 · DOI
  119. 10.1016/j.anai.2019.08.014 · DOI
  120. 10.1016/j.it.2017.01.008 · DOI
  121. 10.1097/ACI.0000000000000234 · DOI
  122. 10.1016/j.jaci.2020.08.001 · DOI
  123. 10.7150/thno.46719 · DOI
  124. 10.1182/blood-2018-02-833582 · DOI
  125. 10.1016/j.immuni.2012.07.007 · DOI · Paper page
  126. 10.1016/j.it.2012.09.008 · DOI · Paper page
  127. 10.1016/j.immuni.2011.03.028 · DOI
  128. 10.1016/j.immuni.2011.09.015 · DOI
  129. 10.1182/blood-2011-03-343962 · DOI · Paper page
  130. 10.1371/journal.pone.0025538 · DOI
  131. 10.1172/JCI75212 · DOI
  132. 10.3389/fimmu.2019.02399 · DOI
  133. 10.1016/j.jaci.2020.01.036 · DOI
  134. 10.18632/oncotarget.11837 · DOI · Paper page
  135. 10.1182/blood-2012-03-415638 · DOI
  136. 10.1002/art.38996 · DOI
  137. 10.1002/jbmr.3234 · DOI · Paper page
  138. 10.1371/journal.pone.0174396 · DOI
  139. 10.7554/eLife.39905 · DOI
  140. 10.1016/j.jaci.2018.04.001 · DOI
  141. 10.1073/pnas.1908816116 · DOI
  142. 10.3389/fimmu.2020.00469 · DOI
  143. 10.1016/j.cmet.2015.04.013 · DOI
  144. 10.1002/JLB.3MA1219-210RR · DOI
  145. 10.1016/j.jaci.2016.01.049 · DOI
  146. 10.1016/j.jaci.2016.04.034 · DOI
  147. 10.1172/JCI138448 · DOI
  148. 10.1159/000506985 · DOI
  149. Ehrlich P, 1878, Beiträge zur Theorie und Praxis der Histologischen Färbung
  150. Jorpes JE, 1937, Über das Vorkommen von Heparin in den Gefäßwänden und in den Augen, Ztschr mikr‐anat Forsch, 42, 279
  151. Holmgren H, 1937, Beitrag zur Kenntnis der Chemie und Funktion der Ehrlichschen Mastzellen, Ztschr mikr‐anat Forsch, 42, 242
  152. Ellis JM, 1949, Urticaria pigmentosa; a report of a case with autopsy, Arch Pathol (Chic), 48, 426
  153. 10.1113/jphysiol.1953.sp004915 · DOI
  154. 10.1038/177427a0 · DOI
  155. Ishizaka K, 1966, Physicochemical properties of reaginic antibody. V. Correlation of reaginic activity with gamma‐E‐globulin antibody, J Immunol, 97, 840
  156. Johansson SG, 1967, Immunological studies of an atypical (myeloma) immunoglobulin, Immunology, 13, 381
  157. Bennich HH, 1968, Immunoglobulin E: a new class of human immunoglobulin, Immunology, 15, 323
  158. Ishizaka T, 1970, The capacity of human immunoglobulin E to mediate the release of histamine and slow reacting substance of anaphylaxis (SRS‐A) from monkey lung, J Immunol, 104, 335, 10.4049/jimmunol.104.2.335 · DOI
  159. Ishizaka T, 1972, Release of histamine and slow reacting substance of anaphylaxis (SRS‐A) by IgE‐anti‐IgE reactions on monkey mast cells, J Immunol, 108, 513, 10.4049/jimmunol.108.2.513 · DOI
  160. 10.1016/S0021-9258(19)68496-6 · DOI · Paper page
  161. 10.4049/jimmunol.126.4.1290 · DOI
  162. Lewis RA, 1982, Prostaglandin D2 generation after sactivation of rat and human mast cells with anti‐IgE, J Immunol, 129, 1627, 10.4049/jimmunol.129.4.1627 · DOI
  163. 10.1016/0092-8674(87)90339-4 · DOI
  164. 10.1073/pnas.84.24.9175 · DOI
  165. 10.1038/337187a0 · DOI
  166. 10.1126/science.2523561 · DOI
  167. 10.1016/0092-8674(90)90280-R · DOI
  168. Kirshenbaum AS, 1992, Effect of IL‐3 and stem cell factor on the apperance of human basophils and mast cells from CD34+ pluripotent progenitor cells, J Immunol, 148, 772, 10.4049/jimmunol.148.3.772 · DOI
  169. 10.1182/blood.V80.9.2237.2237 · DOI · Paper page
  170. 10.1073/pnas.90.2.735 · DOI
  171. 10.1073/pnas.92.23.10560 · DOI
  172. 10.1038/nature03085 · DOI · Paper page
  173. 10.1126/science.1128877 · DOI · Paper page
  174. 10.1016/j.ejphar.2015.04.047 · DOI

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Authors
Dahlin, J. S., Maurer, M., Metcalfe, D. D., Pejler, G., Sagi‐Eisenberg, R., & Nilsson, G.
Affiliations
  • Division of Immunology and Allergy Department of Medicine Karolinska Institutet Karolinska University Hospital Stockholm Sweden
  • Department of Dermatology and Allergy Dermatological Allergology Allergie‐Centrum‐Charité Charité—Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt‐Universität zu Berlin, Berlin Institute of Health Berlin Germany
  • Mast Cell Biology Section Laboratory of Allergic Diseases NIAID, NIH Bethesda MD USA
  • Department of Medical Biochemistry and Microbiology Uppsala University Uppsala Sweden
  • Department of Cell and Developmental Biology Sackler Faculty of Medicine Tel Aviv University Tel Aviv Israel
ORCID
Venue
Allergy
Publisher
Wiley
Published
2021-05-20
Volume
77
Issue
1
Pages
83-99
ISSN
  • 0105-4538
  • 1398-9995
DOI
10.1111/all.14881
Cited by
147
References
11
Language
en
Licence
creativecommons.org/licenses/by-nc-nd/4.0/ (vor)
Funders
  • Cancerfonden
  • Division of Intramural Research, National Institute of Allergy and Infectious Diseases
  • Vetenskapsrådet

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