Fate and Function of CD4+Th Cell Subsets in Autoimmune Diseases
1Zhejiang University, Hangzhou, China
2Jiangsu University, Zhenjiang, China
3Mayo Clinic, Rochester, USA
Fate and Function of CD4+Th Cell Subsets in Autoimmune Diseases
Description
Autoimmune diseases (AID) are a category of complex diseases, characterized by the break-in tolerance and inappropriate activation of the immune system, leading to a shift in the immune system towards a pro-inflammatory state, the production of autoantibodies and tissue destruction. The occurrence and development of AID are closely involved with CD4+T helper (Th) cells such as Th17, Th22, T-regulatory (Treg) cells, and follicular T helper (Tfh) cells, etc.
The CD4+Th cells subsets and their associated immune molecules play crucial roles in the pathogenesis of autoimmune diseases such as systemic lupus erythematosus (SLE), inflammatory bowel diseases (IBD), and rheumatoid arthritis (RA), which will provide novel targets for diagnosis and treatment of AID. Currently, the pathogenesis of AID is very complex and the fate and function of pathogenic CD4+Th cells and associated immune molecules remains unclear and imprecise, including their autophagy, activation, differentiation and apoptosis in AID. Knowledge of the mechanism of CD4+Th cell fate and function will contribute to clinical benefits for AID.
In this Special Issue, we invite researchers to contribute original research articles as well as review articles to discuss new insights and challenges in the fate and function of CD4+Th cells in AID.
Potential topics include but are not limited to the following:
- Mechanism of proliferation and differentiation in CD4+Th cell subsets
- The function and role of CD4+Th cell subsets in autoimmune diseases
- Mechanism of apoptosis, necroptosis, and pyroptosis in CD4+Th cell subsets in autoimmune diseases
- Novel insights in CD4+Th cell subsets fate and function
- The role of early signalling events in fate decision of naïve CD4+T cells towards distinct cell subsets
- Epigenetic regulation of CD4+T cell function