ArticleVirology journal2012
Increased expressions of IL-22 and Th22 cells in the coxsackievirus B3-Induced mice acute viral myocarditis.
Article in Virology journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- Role of HIF-1α-Activated IL-22/IL-22R1/Bmi1 Signaling Modulates the Self-Renewal of Cardiac Stem Cells in Acute Myocardial Ischemia.Stem cell reviews and reports · 2024Article
- Immunopathogenesis and immunomodulatory therapy for myocarditis.Science China. Life sciences · 2023Review
- Decreased frequency of Th22 cells and IL-22 cytokine in kidney transplant patients with active cytomegalovirus infection.BMC immunology · 2023Article
- Alterations of the gut microbiome and metabolic profile in CVB3-induced mice acute viral myocarditis.BMC microbiology · 2023Article
- Current Knowledge of Th22 Cell and IL-22 Functions in Infectious Diseases.Pathogens (Basel, Switzerland) · 2023Review
- Endogenous interleukin-22 prevents cardiac rupture after myocardial infarction in mice.PloS one · 2023Article
- The Role of B Cells in Regulation of Th Cell Differentiation in Coxsackievirus B3-Induced Acute Myocarditis.Inflammation · 2021Article
- Interleukin-22 is elevated in the atrium and plasma of patients with atrial fibrillation and increases collagen synthesis in transforming growth factor-β1-treated cardiac fibroblasts via the JNK pathway.Experimental and therapeutic medicine · 2020Article
- B Cells Increase Myocardial Inflammation by Suppressing M2 Macrophage Polarization in Coxsackie Virus B3-Induced Acute Myocarditis.Inflammation · 2019Article
- The clinical potential of IL-12/IL-35 in treating chemotherapy drug-induced cardiac injury - Authors' reply.EBioMedicine · 2018Article
- Interleukin-22, a potent target for treatment of non-autoimmune diseases.Human vaccines & immunotherapeutics · 2018Article
- Interleukin 22 Promotes Blood Pressure Elevation and Endothelial Dysfunction in Angiotensin II-Treated Mice.Journal of the American Heart Association · 2017Article
- A Critical Role for IL-21 Receptor Signaling in the Coxsackievirus B3-Induced Myocarditis.Inflammation · 2017Article
- Leprosy As a Complex Infection: Breakdown of the Th1 and Th2 Immune Paradigm in the Immunopathogenesis of the Disease.Frontiers in immunology · 2017Review
- Anti-Interleukin-22-Neutralizing Antibody Attenuates Angiotensin II-Induced Cardiac Hypertrophy in Mice.Mediators of inflammation · 2017Article
- The Effects of IL-22 on the Inflammatory Mediator Production, Proliferation, and Barrier Function of HUVECs.Inflammation · 2016Article
- Increased frequency of follicular helper T cells in mice viral myocarditis is relevant with anti-ANT antoantibody.Virology journal · 2015Article
- Interleukin-22 ameliorates liver fibrogenesis by attenuating hepatic stellate cell activation and downregulating the levels of inflammatory cytokines.World journal of gastroenterology · 2015Article
- IL-10-producing B cells involved in the pathogenesis of Coxsackie virus B3-induced acute viral myocarditis.International journal of clinical and experimental pathology · 2015Article
- IL-22-producing Th22 cells play a protective role in CVB3-induced chronic myocarditis and dilated cardiomyopathy by inhibiting myocardial fibrosis.Virology journal · 2014Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRecently, a new subset of T helper (Th) cell that predominantly secret cytokine interleukin-22 (IL-22) is identified, termed Th22 cells. The Th22 subset has been demonstrated to be involved in immunity and tissue inflammation. However, the existence of Th22 cells and role of IL-22 in acute viral myocarditis (AVMC) remain unknown.
methodsBALB/c mice were intraperitoneally (i.p) infected with CVB3 for establishing AVMC models. Control mice were treated with phosphate-buffered saline (PBS) i.p. On day 14 post injection, frequencies of splenic Th22 cells were determined, productions of IL-22 and expressions of IL-22R (IL-22 receptor) were measured. To further investigate the effects of IL-22, AVMC mice treated with Anti-IL-22 neutralizing antibody were explored. The severity of AVMC were monitored; the frequencies of Th22 cells, the expressions of IL-22 and IL-22R were investigated; in addition to IFN-γ, inflammatory cytokines IL-17, TNF-α, IL-6 as well as IL-1β, were evaluated. Cardiac viral replication were detected.
resultsCompared with control group, significant elevations of circulating Th22 cells and IL-22, cardiac protein and mRNA of IL-22, and IL-22R1 were demonstrated in AVMC group. Treatment of AVMC mice with Anti-IL-22 Ab exacerbated the severity of viral myocarditis, verified by lower survival rate, higher HW/BW ratios and cardiac pathological scores. Anti-IL-22 Ab decreased the frequencies of Th22 cells and the levels of IL-22, and increased the expressions of cardiac IL-22R1. Up-regulations of IL-17, IL-6 and TNF-α, down-regulations of IFN-γ proteins and gene expressions in the plasma and myocardium, were observed in Anti-IL-22 Ab group. Furthermore, neutralization of IL-22 significantly promoted cardiac viral replication.
conclusionsOur data indicate that the increased frequencies of IL-22-producing Th22 cells may play an important role in the pathogenesis of CVB3-induced mice AVMC, IL-22 may act as an myocardium-protective cytokine via the IL-22-IL-22R pathway, and suggest that targeting the Th22 cell and IL-22-IL-22R pathway could provide new therapeutic modalities for the treatment of CVB3-induced AVMC.
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