Cutting Edge: Cross-Regulation by TLR4 and T cell Ig Mucin-3 Determines Sex Differences in Inflammatory Heart Disease
Open accessAbstract
Recent clinical studies have reinforced the importance of sex-related differences in the pathogenesis of cardiovascular diseases, with an increased incidence and mortality in men. Similar to humans, male BALB/c mice infected with coxsackievirus B3 (CVB3) develop more severe inflammation in the heart even though viral replication is no greater than in females. We show that TLR4 and IFN-γ levels are significantly elevated and regulatory T cell (Treg) populations significantly reduced in the heart of males following CVB3 infection, whereas females have significantly increased T cell Ig mucin (Tim)-3, IL-4 and Treg. Blocking Tim-3 in males significantly increases inflammation and TLR4 expression while reducing Treg. In contrast, defective TLR4 signaling significantly reduces inflammation while increasing Tim-3 expression. Cross-regulation of TLR4 and Tim-3 occurs during the innate and adaptive immune response. This novel mechanism may help explain why inflammatory heart disease is more severe in males.
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Tim-3 is a receptor upregulated on mast cells and macrophages after viral infection that inhibits T-cell responses and is associated with increased IL-10 release from alternatively activated macrophages.
“Tim-3 (T-cell immunoglobulin mucin domain 3) is a receptor that is upregulated on mast cells and macrophages after viral infection that inhibits T-cell responses and is associated with increased IL-10 release from alternatively activated macrophages. 124,125,146”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [124]
The Innate cross-regulation section (p. 4) reports increased Tim-3 on mast cells and macrophages after CVB3 infection, and the Cross-regulation section (p. 4) links Tim-3 to increased regulatory T-cell populations and reduced inflammation. The cited paper does not report increased IL-10 release from alternatively activated macrophages, so that part of the claim is unsupported. (LLM, conf=0.86)
Experimental — accuracy not yet measuredFew females progress to DCM in humans or autoimmune/viral myocarditis animal models.
“Few females progress to DCM in humans or autoimmune/viral myocarditis animal models. 64,124”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [124]
The introduction (p. 2) says heart disease, including myocarditis, is less common in women, and the Results and Discussion (p. 3) report less acute viral myocarditis in female than male mice. The introduction also says the mouse model can progress to dilated cardiomyopathy, but the paper does not establish that few females progress to it in humans or in autoimmune or viral myocarditis models. (LLM, conf=0.85)
Experimental — accuracy not yet measuredMast cells are the first APCs to respond to CVB3 within 15 minutes of intraperitoneal infection during autoimmune CVB3 myocarditis, leading to upregulation of TLR4, and this response leads to rapid increases in TNF, IL-1β, IL-6, and IFNγ in many organs including the heart.
“We showed that mast cells are the first APCs to respond to CVB3 within 15 minutes of intraperitoneal infection during autoimmune CVB3 myocarditis, leading to upregulation of TLR4, and that this response leads to rapid increases in TNF, IL-1 β , IL-6, and IFN γ in many organs including the heart. 124,146,160”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [124]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredMen develop more scar tissue and dilated cardiomyopathy (DCM) than women.
“with men developing more scar tissue and dilated cardiomyopathy (DCM) than women. 64,124,131”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [124]
The Results and Discussion (p. 3) report more severe acute myocarditis in male than female mice. The introduction (p. 2) says this model can progress to dilated cardiomyopathy, but does not compare that outcome by sex; our copy also does not report a sex comparison for scar tissue. Thus, the paper supports a related sex difference in inflammation, not the two outcomes claimed. (LLM, conf=0.84)
Experimental — accuracy not yet measuredMen have more neutrophils and monocytes, whereas women have more T cells, similar to autoimmune myocarditis.
“And men have more neutrophils and monocytes, whereas women have more T cells, 13,121-123 similar to autoimmune myocarditis. 124,125”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [124]
In Results and Discussion (p. 3), the paper reports more monocyte/macrophages and granulocytes in male mice with CVB3-induced myocarditis. It reports more B cells and specific regulatory T-cell populations in females, but does not establish that females have more T cells overall. The findings are in mice, not men and women. (LLM, conf=0.86)
Experimental — accuracy not yet measured
The TLR4, caspase-1, and NLRP3 pathways are upregulated in patients, EAM, autoimmune CVB3 myocarditis, and CVB3-only models and increase IL-1β and IL-18 levels in the heart.
“Another key pathway upregulated in patients, EAM, autoimmune CVB3 myocarditis, and CVB3only models is the TLR4, caspase-1, and NLRP3 pathways that increase IL-1 β and IL-18 levels in the heart. 124,146,152,156,161-164”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [124]
The introduction (p. 2) reports that TLR4 signaling increases cardiac IL-1β and IL-18 after CVB3 infection in male BALB/c mice, and Results and Discussion (p. 3) finds increased TLR4 expression on cardiac macrophages from males. The paper does not establish caspase-1 or NLRP3 upregulation, or extend these findings to patients, EAM, or CVB3-only models; its mouse inoculum contained both virus and cardiac myosin. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe majority of immune cells in the heart during acute myocarditis in EAM, autoimmune CVB3 myocarditis model, and humans are CD11b+ cells that include neutrophils, macrophages, mast cells, and some dendritic cells.
“The majority of immune cells in the heart during acute myocarditis in EAM, the autoimmune CVB3 myocarditis model, and humans are CD11b+ cells that include neutrophils, macrophages, mast cells, and some dendritic cells. 124,146,152,159”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [124]
The Results and Discussion (p. 3) identify CD11b+ heart inflammation during acute CVB3-induced myocarditis in mice and say it includes macrophages, granulocytes, and mast cells. The paper does not establish that CD11b+ cells are a majority of infiltrating immune cells, include dendritic cells in that group, or predominate in EAM or human myocarditis. (LLM, conf=0.88)
Experimental — accuracy not yet measuredElevated TLR4 and IL-1β are found on CD11b/CR3-expressing macrophages and mast cells during the innate immune response in the spleen and heart and in the heart during acute myocarditis.
“Importantly, elevated TLR4 and IL-1 β are found on CD11b/CR3-expressing macrophages and mast cells during the innate immune response in the spleen and heart and in the heart during acute myocarditis. 124,146”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [124]
Results and Discussion (p. 3) reports increased TLR4 on cardiac macrophages and, in several experiments, mast cells during acute myocarditis; it also reports higher IL-1β levels in males. Innate cross-regulation (pp. 4–5) reports increased TLR4 on these cells and mentions similar expression findings in the spleen. The paper does not show elevated IL-1β on those cells, identify them as CR3-expressing, or establish the full claimed combination in both spleen and heart. (LLM, conf=0.87)
Experimental — accuracy not yet measuredType I and II IFNs are a dominant immune response in CVB3 myocarditis models and EAM, where inhibition of these pathways leads to increased viral replication, pericardial and myocardial inflammation, and DCM.
“Type I and II IFNs are a dominant immune response in CVB3 myocarditis models (and EAM) where inhibition of these pathways leads to increased viral replication, pericardial and myocardial inflammation, and DCM. 124,128,152,169,170”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [124]
The Results and Discussion (p. 3) report higher IFN-γ in male mice with CVB3 myocarditis, and the introduction (p. 2) says this model can progress to dilated cardiomyopathy. The paper does not establish a dominant type I and II IFN response in CVB3 myocarditis and EAM, or show that inhibiting those pathways increases viral replication, pericardial or myocardial inflammation, or DCM. (LLM, conf=0.84)
Experimental — accuracy not yet measuredTim-3 is an important regulator of T cells following TLR4 activation and displays sex differences during CVB3 myocarditis.
“An important regulator of T cells following TLR4 activation is Tim-3, which displays sex differences during CVB3 myocarditis. 124,125,146”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [124]
This time course is the same as observed with the autoimmune CVB3 and murine cytomegalovirus models of myocarditis and EAM.
“This time course is the same as is observed with the autoimmune CVB3 and murine cytomegalovirus models of myocarditis and EAM (Table S1). 35,124,170,188”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [124]
The accuracy of cMRI depends on the amount of scar tissue present.
“The accuracy of cMRI depends on the amount of scar tissue present”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [124]
The Results and Discussion (p. 3) describe histological assessment of inflammation in mouse hearts, while the methods (p. 2) describe plaque assays and cell analysis. Searches for cMRI, scar tissue, and cardiac magnetic resonance imaging found no passage addressing whether scar amount affects cMRI accuracy. (LLM, conf=0.78)
Experimental — accuracy not yet measured
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Epidemiological Impact of Myocarditis
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“While males present with increased γδ T cells; increased TLR4+ CD11b+ inflammation, including macrophages, neutrophils, mast cells and DCs; and an increased Th1 response, females present with protective Th2 response, increased B cells, more inhibitory Tim-3+ CD4+ T cells and more T regulatory cells [96,97].”
BackgroundUchida, Y., Ke, B., Freitas, M. C. S., Yagita∥, H., Akiba, H., Busuttil, R. W., Najafian, N., & Kupiec‐Weglinski, J. W. (2010) · Gastroenterology · doi:10.1053/j.gastro.2010.07.003 · Cited by 119 · see citing works
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Sex Differences in Destructive Periodontal Disease: Exploring the Biologic Basis
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Self-citationGender differences in autoimmunity associated with exposure to environmental factors
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“The same group also found that sex related differences in BALB/c mice also included elevated TLR4 and reducedTreg inmalemice and increased IL-4 andTreg in femalemice [153].”
BackgroundBondue, A., Arbustini, E., Bianco, A., Ciccarelli, M., Dawson, D. K., Rosa, M. D., Hamdani, N., Hilfiker‐Kleiner, D., Meder, B., Leite-Moreira, A. F., et al. (2018) · Cardiovascular Research · doi:10.1093/cvr/cvy122 · Cited by 103 · see citing works
Elevated Sera sST2 Is Associated With Heart Failure in Men ≤50 Years Old With Myocarditis
Coronado, M. J., Bruno, K. A., Blauwet, L. A., Tschöpe, C., Cunningham, M. W., Pankuweit, S., van Linthout, S., Jeon, E., McNamara, D. M., Krejčí, J., et al. (2019) · Journal of the American Heart Association · doi:10.1161/jaha.118.008968 · Cited by 99 · see citing works
“Previously we reported that CD11b, TLR4, caspase-1, and IL-1b are increased by testosterone in male mice with myocarditis.(7,8,20,42)”
BackgroundResultInfluentialSelf-citationRegulation of dendritic cell differentiation and function by estrogen receptor ligands
Kovats, S., & Carreras, E. (2008) · Cellular Immunology · doi:10.1016/j.cellimm.2007.10.008 · Cited by 95 · see citing works
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“Discussion Proinflammatory Th1 and Th17 immune responses are known to be important in the pathogenesis of experimental autoimmune myocarditis (EAM) and autoimmune CVB3 myocarditis mouse models [25–27].”
BackgroundSelf-citationTim-3 Directly Enhances CD8 T Cell Responses to Acute Listeria monocytogenes Infection
Gorman, J. V., Starbeck-Miller, G. R., Pham, N., Traver, G. L., Rothman, P. B., Harty, J. T., & Colgan, J. D. (2014) · The Journal of Immunology · doi:10.4049/jimmunol.1302290 · Cited by 90 · see citing works
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“2008) and is critical to some animal models of auto immunity (Frisancho-Kiss et al. 2007).”
BackgroundSelf-citationT cell co-stimulation and co-inhibition in cardiovascular disease: a double-edged sword
Simons, K. H., de Jong, A., Jukema, J. W., de Vries, M. R., Arens, R., & Quax, P. H. A. (2019) · Nature Reviews Cardiology · doi:10.1038/s41569-019-0164-7 · Cited by 88 · see citing works
Sex Differences in Cardiomyopathies
Meyer, S., van der Meer, P., van Tintelen, J. P., & van den Berg, M. P. (2014) · European Journal of Heart Failure · doi:10.1002/ejhf.15 · Cited by 86 · see citing works
Sex Differences in Susceptibility to Viral Infection
Klein, S. L., & Huber, S. A. (2009) · Springer eBooks · doi:10.1007/978-3-642-02155-8_4 · Cited by 86 · see citing works
Shakti, D., Hehn, R. S., Gauvreau, K., Sundel, R. P., & Newburger, J. W. (2014) · Journal of the American Heart Association · doi:10.1161/jaha.114.001483 · Cited by 85 · see citing works
Batton, K. A., Austin, C. O., Bruno, K. A., Burger, C. D., Shapiro, B. P., & Fairweather, D. (2018) · Biology of Sex Differences · doi:10.1186/s13293-018-0176-8 · Cited by 81 · see citing works
“Transforming growth factor (TGF)-β1 promotes collagen deposition while Toll-like receptor (TLR) 4-induced IL-1β and IL-18 enhance remodeling associated with VSMCs [103].”
BackgroundSelf-citationRegulation of T cell responses by the receptor molecule Tim-3
Gorman, J. V., & Colgan, J. D. (2014) · Immunologic Research · doi:10.1007/s12026-014-8524-1 · Cited by 81 · see citing works
Current treatment options in (peri)myocarditis and inflammatory cardiomyopathy
Maisch, B., & Pankuweit, S. (2012) · Herz · doi:10.1007/s00059-012-3679-9 · Cited by 80 · see citing works
TRIF Is a Critical Survival Factor in Viral Cardiomyopathy
Riad, A., Westermann, D., Zietsch, C., Savvatis, K., Becher, P. M., Bereswill, S., Heimesaat, M. M., Lettau, O., Laßner, D., Dörner, A., et al. (2011) · The Journal of Immunology · doi:10.4049/jimmunol.1002029 · Cited by 79 · see citing works
Unresolved issues in theories of autoimmune disease using myocarditis as a framework
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Self-citationTIM-3: A Novel Regulatory Molecule of Alloimmune Activation
Boenisch, O., D’Addio, F., Watanabe, T., Elyaman, W., Magee, C. N., Yeung, M. Y., Padera, R. F., Rodig, S. J., Murayama, T., Tanaka, K., et al. (2010) · The Journal of Immunology · doi:10.4049/jimmunol.0903435 · Cited by 76 · see citing works
Autoimmune heart disease: role of sex hormones and autoantibodies in disease pathogenesis
Fairweather, D., Petri, M., Coronado, M. J., & Cooperr, L. T. (2012) · Expert Review of Clinical Immunology · doi:10.1586/eci.12.10 · Cited by 74 · see citing works
Self-citationType B Coxsackieviruses and Their Interactions with the Innate and Adaptive Immune Systems
Kemball, C. C., Alirezaei, M., & Whitton, J. L. (2010) · Future Microbiology · doi:10.2217/fmb.10.101 · Cited by 74 · see citing works
“myocarditis [16].”
TIM-1 and TIM-3 proteins in immune regulation
Su, E. W., Lin, J., & Kane, L. (2008) · Cytokine · doi:10.1016/j.cyto.2008.06.013 · Cited by 73 · see citing works
“The authors compared the levels of Tim-3 on infected male and female BALB/c mice and found that there was significantly less Tim-3 on mast cells, macrophages and CD4 T cells isolated from the hearts of CVB3-infected male mice [53].”
BackgroundBruno, K. A., Mathews, J. E., Yang, A. L., Frisancho, J. A., Scott, A. J., Greyner, H. D., Molina, F. A., Greenaway, M. S., Cooper, G. M., Bucek, A., et al. (2019) · Frontiers in Endocrinology · doi:10.3389/fendo.2019.00598 · Cited by 73 · see citing works
“, TLR4, caspase-1, IL-1β, and IL-18) are upregulated in the heart during viral myocarditis in male mice and that testosterone elevates this pathway on mast cells and macrophages during the innate and adaptive immune response to CVB3 infection in our model (44, 46).”
BackgroundMethodInfluentialSelf-citationMyocarditis associated with COVID-19 vaccination
Buoninfante, A., Andeweg, A. C., Genov, G., & Cavaleri, M. (2024) · npj Vaccines · doi:10.1038/s41541-024-00893-1 · Cited by 76 · see citing works
Abston, E. D., Barin, J. G., Cihakova, D., Bucek, A., Coronado, M. J., Brandt, J. E., Bedja, D., Kim, J. B., Georgakopoulos, D., Gabrielson, K. L., et al. (2012) · Circulation: Heart Failure · doi:10.1161/circheartfailure.111.963769 · Cited by 69 · see citing works
“rIL-33 increases cardiac IL-33, IL-4, IL-1 IL-6 and serum sST2, and alters remodeling during acute CVB3 myocarditis IL-33 has been demonstrated to promote Th2 responses.(12,25,29) For this reason we examined the effect of rIL-33 or rST2 treatment on Th2-associated cytokines in the heart (e.”
Self-citationWang, S., Cao, C., Piao, H., Li, Y., Yu, T., Zhang, X., Zhang, D., Sun, C., Zhu, R., Wang, Y., et al. (2015) · Scientific Reports · doi:10.1038/srep09013 · Cited by 65 · see citing works
Autoimmune Myocarditis, Valvulitis, and Cardiomyopathy
Myers, J. M., Fairweather, D., Huber, S. A., & Cunningham, M. W. (2013) · Current Protocols in Immunology · doi:10.1002/0471142735.im1514s101 · Cited by 63 · see citing works
“Male BALB/c mice develop more severe acute and chronic myocarditis/DCM than females (Frisancho-Kiss et al., 2007, 2009; Onyimba et al., 2011; Coronado et al., 2012).”
BackgroundSelf-citationTim-3: Expression on immune cells and roles at the maternal-fetal interface
Hu, X., Tang, M., Mor, G., & Liao, A. (2016) · Journal of Reproductive Immunology · doi:10.1016/j.jri.2016.10.113 · Cited by 57 · see citing works
Sex-specific environmental influences on the development of autoimmune diseases
Tiniakou, E., Costenbader, K. H., & Kriegel, M. A. (2013) · Clinical Immunology · doi:10.1016/j.clim.2013.02.011 · Cited by 56 · see citing works
“Interestingly, antiphospholipid antibodies can be induced by estrogen in mice [74, 78], but a link between sex, microbial agents and antiphospholipid syndrome has not yet been established.”
BackgroundOnyimba, J. A., Coronado, M. J., Garton, A. E., Kim, J. B., Bucek, A., Bedja, D., Gabrielson, K. L., Guilarte, T. R., & Fairweather, D. (2011) · Biology of Sex Differences · doi:10.1186/2042-6410-2-2 · Cited by 57 · see citing works
“More severe disease in males is associated with increased Toll-like receptor (TLR)4 expression on mast cells and macrophages in the heart during acute myocarditis and in the spleen at 12 h pi [12-14].”
BackgroundInfluentialSelf-citationCardiomyopathies: Classification, Diagnosis, and Treatment
Maisch, B., Noutsias, M., Ruppert, V., Richter, A., & Pankuweit, S. (2011) · Heart Failure Clinics · doi:10.1016/j.hfc.2011.08.014 · Cited by 55 · see citing works
Roberts, B. J., Dragon, J. A., Moussawi, M., & Huber, S. A. (2012) · Biology of Sex Differences · doi:10.1186/2042-6410-3-25 · Cited by 54 · see citing works
“While microarray analysis showed sex differences in TLR2 expression, a role for TLR4 in CVB3 myocarditis has also been shown [25-27].”
BackgroundResultMaisch, B., & Pankuweit, S. (2012) · Heart Failure Reviews · doi:10.1007/s10741-012-9362-7 · Cited by 53 · see citing works
Roberts, B. J., Moussawi, M., & Huber, S. A. (2012) · Experimental and Molecular Pathology · doi:10.1016/j.yexmp.2012.06.005 · Cited by 54 · see citing works
Sex-related Differences in Mast Cell Activity and Doxorubicin Toxicity
Zhang, J., Knapton, A. D., Lipshultz, S. E., Cochran, T. R., Hiraragi, H., & Herman, E. H. (2013) · Toxicologic Pathology · doi:10.1177/0192623313482778 · Cited by 53 · see citing works
“Mast cells (MCs) and macrophages contain estrogen and androgen receptors (Frisancho-Kiss et al. 2007).”
BackgroundDistinct Th17 inductions contribute to the gender bias in CVB3-induced myocarditis
Li, Z., Yue, Y., & Xiong, S. (2013) · Cardiovascular Pathology · doi:10.1016/j.carpath.2013.02.004 · Cited by 52 · see citing works
Clinical Characteristics and Mechanisms of Acute Myocarditis
Heymans, S. R. B., Linthout, S. V., Kraus, S., Cooper, L. T., & Ntusi, N. (2024) · Circulation Research · doi:10.1161/circresaha.124.324674 · Cited by 52 · see citing works
“52 Beyond the impact of biological sex on the immune response and viral myocarditis, the genetic background is of relevance in myocarditis, as outlined below.”
BackgroundAutoimmunity in viral myocarditis
Reddy, J., Massilamany, C., Buskiewicz, I., & Huber, S. A. (2013) · Current Opinion in Rheumatology · doi:10.1097/bor.0b013e3283620036 · Cited by 50 · see citing works
The Toll-Like Receptor Radical Cycle Pathway: A New Drug Target in Immune-Related Chronic Fatigue
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Testosterone, cardiomyopathies, and heart failure
Diaconu, R., Donoiu, I., Mirea, O., & Bălşeanu, T. A. (2021) · Asian Journal of Andrology · doi:10.4103/aja.aja_80_20 · Cited by 51 · see citing works
Abston, E. D., Coronado, M. J., Bucek, A., Onyimba, J. A., Brandt, J. E., Frisancho, J. A., Kim, E., Bedja, D., Sung, Y.-K., Radtke, A. J., et al. (2012) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00516.2011 · Cited by 48 · see citing works
Self-citationSex-Specific Differences of the Inflammatory State in Experimental Autoimmune Myocarditis
Barcena, M. L., Jeuthe, S., Niehues, M. H., Pozdniakova, S., Haritonow, N., Kühl, A. A., Messroghli, D. R., & Regitz-Zagrosek, V. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.686384 · Cited by 47 · see citing works
Intricacies of cardiac damage in coxsackievirus B3 infection: Implications for therapy
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“Furthermore, expression of TLRs can occur gender dependently: elevated expression of TLR-4 in the macrophages of male mice contributed to mortalities in CVB3infected animals, but the underlying mechanisms are unknown [70, 71].”
BackgroundNyland, J. F., Fairweather, D., Shirley, D. L., Davis, S., Rose, N. R., & Silbergeld, E. K. (2011) · Toxicological Sciences · doi:10.1093/toxsci/kfr264 · Cited by 47 · see citing works
“Male BALB/cJ (BALB/c) mice (6–8 weeks old; The Jackson Laboratory) were used in this study because myocarditis and DCM are more prevalent in men (Roger et al., 2011) and male BALB/c mice develop more severe myocarditis and DCM (Frisancho-Kiss et al., 2006, 2007).”
BackgroundMethodSelf-citationSex Differences, Genetic and Environmental Influences on Dilated Cardiomyopathy
Jain, A., Norton, N., Bruno, K. A., Cooper, L. T., Atwal, P. S., & Fairweather, D. (2021) · Journal of Clinical Medicine · doi:10.3390/jcm10112289 · Cited by 46 · see citing works
Self-citationLiu, L., Yue, Y., & Xiong, S. (2014) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2014.07.021 · Cited by 46 · see citing works
“Actually, similar results have also been reported by other groups [6,61].”
BackgroundResultZhang, Z. (2010) · Oncology Reports · doi:10.3892/or_00000909 · Cited by 46 · see citing works
Riad, A., Westermann, D., Escher, F., Becher, P. M., Savvatis, K., Lettau, O., Heimesaat, M. M., Bereswill, S., Volk, H., Schultheiß, H., et al. (2010) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.01188.2009 · Cited by 44 · see citing works
(2022) · doi:10.1016/j.isci.2022.103865 · Cited by 43 · see citing works
“On the other hand, the Th2 cells could attenuate acute myocarditis (Frisancho-Kiss et al., 2007; Liu and Huber, 2011) but can also promote cardiac remodeling events, leading to chronic myocarditis/DCM associated with cardiac fibrosis (Abston et al.”
BackgroundQi, X., Xu, J., Wang, F., & Xiao, J. (2012) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2012/162934 · Cited by 43 · see citing works
“Therefore, increased cholesterol metabolism associated with TSPO during the immune response to CVB3 infection may drive the proinflammatory reaction of myocarditis [81, 82].”
BackgroundThe sex and gender dimensions of COVID-19: A narrative review of the potential underlying factors
Mourosi, J. T., Anwar, S., & Hosen, M. J. (2022) · Infection Genetics and Evolution · doi:10.1016/j.meegid.2022.105338 · Cited by 45 · see citing works
Innate and adaptive immune responses against picornaviruses and their counteractions: An overview
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Fairweather, D., Coronado, M. J., Garton, A. E., Dziedzic, J. L., Bucek, A., Cooper, L. T., Brandt, J. E., Alikhan, F. S., Wang, H., Endres, C. J., et al. (2014) · Journal of Cardiovascular Translational Research · doi:10.1007/s12265-013-9538-0 · Cited by 39 · see citing works
“Previously, we showed in a mouse model of CVB3myocarditis that testosterone increases CD11b expression on cardiac macrophages during acute myocarditis in male mice [24, 25].”
BackgroundMethodInfluentialSelf-citationSex Hormone Receptor Expression in the Immune System
Buskiewicz, I. A., Huber, S. A., & Fairweather, D. (2016) · Elsevier eBooks · doi:10.1016/b978-0-12-802388-4.00004-5 · Cited by 38 · see citing works
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Coagulation, Protease-Activated Receptors, and Viral Myocarditis
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Influence of Cinnamaldehyde on Viral Myocarditis in Mice
Ding, Y., Wang, S., Qiu, L., Gangtao, Z., & Jing-feng, X. (2010) · The American Journal of the Medical Sciences · doi:10.1097/maj.0b013e3181dd3b43 · Cited by 36 · see citing works
Sexual dimorphisms of mRNA and miRNA in human/murine heart disease
Tsuji, M., Kawasaki, T., Matsuda, T., Arai, T., Gojo, S., & Takeuchi, J. (2017) · PLoS ONE · doi:10.1371/journal.pone.0177988 · Cited by 34 · see citing works
Clinical Presentation and Laboratory Findings in Men Versus Women with Myocarditis
Patriki, D., Kottwitz, J., Berg, J., Landmesser, U., Lüscher, T. F., & Heidecker, B. (2019) · Journal of Women s Health · doi:10.1089/jwh.2018.7618 · Cited by 34 · see citing works
- Authors
- Frisancho-Kiss, S., Davis, S. E., Nyland, J. F., Frisancho, J. A., Cihakova, D., Barrett, M. A., Rose, N. R., & Fairweather, D.
- Affiliations
- Department of Environmental Health Sciences, Johns Hopkins University, Bloomberg School of Public Health and School of Medicine , Baltimore, MD 21205
- Johns Hopkins University (US)
- Department of Pathology, Johns Hopkins University, Bloomberg School of Public Health and School of Medicine , Baltimore, MD 21205
- Corresponding author
- Fairweather, DeLisa
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2007-06-01
- Volume
- 178
- Issue
- 11
- Pages
- 6710-6714
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1500123828
- Cited by
- 212
- References
- 24
- Citations by year
- 2026: 10 · 2025: 7 · 2024: 11 · 2023: 17 · 2022: 13 · 2021: 9 · 2020: 9 · 2019: 10 · 2018: 6 · 2017: 7 · 2016: 7 · 2015: 11 · 2014: 19 · 2013: 13 · 2012: 23
- FWCI
- 3.92
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL087033, HL077611, HL 70729, R01HL070729, HL087033)
- National Institute of Environmental Health Sciences (ES03819, P30ES003819, T32ES007141)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Viral Infections and Immunology Research
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- sex differences, inflammatory heart disease, TLR4, TIM-3, coxsackievirus B3, myocarditis, regulatory T cells, interferon-gamma, IL-4, innate and adaptive immunity, viral infection, cardiac inflammation
- MeSH terms
- Hepatitis A Virus Cellular Receptor 2, Animals, Coxsackievirus Infections, Female, Macrophages, Male, Mast Cells, Mice, Inbred BALB C, Mice, Transgenic, Myocarditis, Receptors, Virus, Sex Characteristics, Signal Transduction, Up-Regulation, Mice, Knockout, Receptor Cross-Talk, Enterovirus B, Human, Toll-Like Receptor 4, Mice
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