ArticleVirology journal2014
IL-22-producing Th22 cells play a protective role in CVB3-induced chronic myocarditis and dilated cardiomyopathy by inhibiting myocardial fibrosis.
Article in Virology journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- IL-22 Exacerbates Coxsackievirus Type B3-Induced Pancreatitis by Elevating Viral Replication Through STAT3 Activation.Immune network · 2025Article
- The roles of Th cells in myocardial infarction.Cell death discovery · 2024Review
- Innate and adaptive immunity in acute myocarditis.International journal of cardiology · 2024Review
- Review
- Immunopathogenesis and immunomodulatory therapy for myocarditis.Science China. Life sciences · 2023Review
- The Molecular Role of Immune Cells in Dilated Cardiomyopathy.Medicina (Kaunas, Lithuania) · 2023Review
- Identification of key immune-related genes in dilated cardiomyopathy using bioinformatics analysis.Scientific reports · 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
- IL-22 inhibits bleomycin-induced pulmonary fibrosis in association with inhibition of IL-17A in mice.Arthritis research & therapy · 2022Article
- Circulating c-Met-Expressing Memory T Cells Define Cardiac Autoimmunity.Circulation · 2022Article
- A nonredundant role for T cell-derived interleukin 22 in antibacterial defense of colonic crypts.Immunity · 2022Article
- Urokinase-loaded cyclic RGD-decorated liposome targeted therapy forFrontiers in bioengineering and biotechnology · 2022Article
- Attenuated strain of CVB3 with a mutation in the CAR-interacting region protects against both myocarditis and pancreatitis.Scientific reports · 2021Article
- Friend or foe of innate lymphoid cells in inflammation-associated cardiovascular disease.Immunology · 2021Review
- QiShenYiQi pill improves the reparative myocardial fibrosis by regulating autophagy.Journal of cellular and molecular medicine · 2020Article
- 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
- Interleukin-22 Inhibits Respiratory Syncytial Virus Production by Blocking Virus-Mediated Subversion of Cellular Autophagy.iScience · 2020Article
- Picornavirus Cellular Remodeling: Doubling Down in Response to Viral-Induced Inflammation.Current clinical microbiology reports · 2020Article
- IL-22 produced by Th22 cells aggravates atherosclerosis development in ApoEJournal of cellular and molecular medicine · 2020Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA new subset of T helper (Th) cells, named IL-22-producing Th22 cells, was identified recently. Th22 cells have been implicated in immunity and inflammation. However, the role of these cells in the progression from acute viral myocarditis (AVMC) to dilated cardiomyopathy (DCM) and myocardial fibrosis remains unknown.
methodsBALB/c mice were repeatedly i.p. infected with Coxsackie virus B3 (CVB3) to establish models of AVMC, chronic myocarditis and DCM. On week 2, 12 and 24 post initial injection, the percentage of splenic Th22 cells, the levels of plasma IL-22, cardiac IL-22 receptor (IL-22R) expression, and indicators of myocardial fibrosis were measured. Further, mice with AVMC and chronic myocarditis were treated with an anti-IL-22 neutralizing antibody (Ab). The collagen volume fraction (CVF), the percentage of splenic Th22 cells, plasma IL-22 levels, cardiac IL-22R expression and indicators of myocardial fibrosis were then monitored.
resultsCompared to control mice at the same time points, AVMC, chronic myocarditis and DCM mice have higher percentage of splenic Th22 cells, higher plasma IL-22 levels, increased cardiac IL-22R, as well as increased collagen typeI-A1 (COL1-A1), collagen type III-A1 (COL3-A1) and matrix metalloproteinase-9 (MMP9) expression. However, the expression of tissue inhibitor of metalloproteinase-1(TIMP-1) was decreased. Treatment of AVMC and chronic myocarditis mice with an anti-IL-22 Ab decreased the survival rate and exacerbated myocardial fibrosis. The percentage of splenic Th22 cells, plasma IL-22 levels and cardiac IL-22R expression also decreased in anti-IL-22 Ab treatment group as compared to IgG and PBS treated groups of AVMC and chronic myocarditis mice. Moreover, increased expression of COL1-A1, COL3-A1, MMP9 but decreased expression of TIMP-1 were observed in anti-IL-22 Ab mouse group.
conclusionsTh22 cells play an important role in the pathogenesis of CVB3-induced mouse chronic myocarditis and DCM. IL-22 is a myocardium-protective cytokine by inhibiting myocardial fibrosis. Therefore, Th 22 cells may be considered as potential therapeutic targets for DCM.
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