Related Experiment Video
Updated: Jun 1, 2026

Accessing Early Differentiation of Virus-Specific Follicular Helper CD4+ T Cell in Acute LCMV-Infected Mice
Published on: April 26, 2024
Distinct different expression of Th17 and Th9 cells in coxsackie virus B3-induced mice viral myocarditis
Kong Qing1, Wu Weifeng, Yang Fan
1Guangxi Cardiovascular Institute, Shuang-Yong Road, Nanning, China.
Insights
This study found that Th17 cells, not Th9 cells, are elevated in viral myocarditis (VMC) models. Th9 cells do not appear to play a role in VMC development or protection.
Area of Science:
- Immunology
- Pathogenesis of Viral Myocarditis
Background:
- Th9 cells, a CD4+ T helper subset secreting IL-9, are implicated in inflammation and autoimmune diseases.
- Th17 cells are known to be critical in viral myocarditis (VMC).
- The role of Th9 cells in VMC pathogenesis remains unclear.
Purpose of the Study:
- To investigate the involvement of Th9 cells in the pathogenesis of coxsackievirus B3 (CVB3)-induced viral myocarditis (VMC).
Main Methods:
- Established VMC models in BALB/c mice using CVB3 infection.
- Analyzed myocardial histopathology, splenic Th17 and Th9 cell frequencies via flow cytometry.
- Quantified cardiac IL-17 and IL-9 mRNA levels using RT-PCR and nested PCR.
Main Results:
- Th17 cell levels and IL-17 mRNA significantly increased in VMC mice post-infection, peaking at day 28 and persisting.
- Th9 cell frequencies and IL-9 mRNA showed no significant difference between VMC and control groups.
- Myocardial histopathological changes were observed in VMC mice.
Conclusions:
- Th17 cells, but not Th9 cells, are significantly elevated during CVB3-induced VMC.
- The VMC microenvironment favors Th17 cell differentiation and proliferation over Th9 cells.
- Preliminary data suggest Th9 cells neither protect against nor promote VMC.
Background:
Recently, a new subset of CD4+T helper(Th) cell that predominantly secret cytokine interleukin-9(IL-9) is identified, termed Th9 cell. It has been reported to participate in tissue inflammation and autoimmune responses, and induce disease which differed from Th17 cells. Th17 cells have been shown to play a critical role in viral myocarditis (VMC), but whether Th9 cells are involved in the pathogenesis of VMC remains unclear.
Results:
BALB/c mice were intraperitoneally (i.p) injected with coxsackie virus B3(CVB3) for establishing VMC models. Control mice were treated with phosphate-buffered saline i.p. On day 0,7,14,21,28,35,42 after injection, myocardial histopathological changes were evaluated by hematoxylin-eosin staining. Splenic Th17 and Th9 cells subsets were analyzed by flow cytometry. And cardiac IL-17, IL-9 mRNA were measured by semi-quantitative reverse transcription-PCR and nested PCR, respectively. Results showed the levels of Th17 cells and IL-17 mRNA obviously increased in VMC mice on 7 day after infection, peaked on day 28, and highly persisted to at least day 42 (p < 0.05). While the frequencies of Th9 cells and IL-9 mRNA showed no significant difference between VMC and control group throughout the course of the experiment(p > 0.05).
Conclusions:
It was differentiated Th17 but not Th9 cells significantly elevated in the development of CVB3-induced VMC. The microenvironment of VMC seemed to contribute to the differentiation and proliferation of Th17 rather than Th9 cells. Our preliminary data implied Th9 cells could not protect against VMC nor promote the disease.
More Related Videos
07:17Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice
Published on: June 22, 2016
10:39In Vitro Analysis of Myd88-mediated Cellular Immune Response to West Nile Virus Mutant Strain Infection
Published on: November 27, 2014