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. 2023 Jul 11;14:1198365. doi: 10.3389/fimmu.2023.1198365

Figure 3.

Figure 3

Pathophysiological aspects of autoimmune diseases are influenced by CTLA-4. (A) Expression of CTLA-4 in the T conventional and T regulatory cells (CD+FoxP3+) can inhibit the pathogenesis of RA. (B) CTLA-4 expression attenuates the Treg cell’s immune suppressive function and inhibits the CD8+ CD28+ T-cell functions that affect B-cell production of autoantibodies during SLE pathogenesis. (C) The CTLA4 signaling molecule can activate Treg cells and reduce MS activity. (D) CTLA-4 differentiates the CD4+CD25+ Treg cells and inhibits T1D pathogenesis by increasing the secretion of IL-10 and TGF-β. Additionally, CTLA-4 interaction with macrophages reduces pro-inflammatory cytokine (IL-1 and IFN-γ) secretion and inhibits T1D. (E) In MG, CTLA-4 expression decreases the frequency of Th1 and Th17 cells and their cytokine production. (F) In AITD, the CTLA-4 plays an inhibitory role by activating the CD4+CD25+ Treg cells and their immunosuppressive functions.