Fig. 8: TIGIT controls muscle inflammation by regulating Th1 and Th17 cell differentiation epigenetically in EAM. | Nature Communications

Fig. 8: TIGIT controls muscle inflammation by regulating Th1 and Th17 cell differentiation epigenetically in EAM.

From: TIGIT deficiency promotes autoreactive CD4+ T-cell responses through a metabolic‒epigenetic mechanism in autoimmune myositis

Fig. 8: TIGIT controls muscle inflammation by regulating Th1 and Th17 cell differentiation epigenetically in EAM.The alternative text for this image may have been generated using AI.

a Naive CD4+ T cells from Tigit+/+ or Tigit−/− mice were adoptively transferred into Rag1−/− mice. EAM was induced as shown in Fig. 2 and treated with C646 (10 mg/kg/d) or vehicle. b–f T-bet, RORγt, IFNγ, and IL-17A expression in CD4+ T cells from the spleens of Tigit+/+ or Tigit−/− mice was measured by flow cytometry. g, h FoxP3 expression in CD4+ T cells was measured by flow cytometry. i NCG mice were immune reconstituted with PBMCs from five independent HC or PM patients. Four weeks later, the mice were treated with C646 (10 mg/kg/d) for 2 weeks. j Muscle strength of mice that received HC or PM PBMCs treated with vehicle or C646. k HE staining and histological score of muscle (quadriceps) sections from mice that received HC or PM PBMCs treated with vehicle or C646. Original magnification: ×100. l, m Image showing spleen size in mice that received HC or PM PBMCs treated with vehicle or C646. Spleen weight index was calculated by dividing spleen weight (mg) by body weight (g). n, o IFNγ and IL-17A expression in CD4+ T cells from the spleen was measured by flow cytometry. c, d, f, h n = four biologically independent replicates. j, k, m, n n = five biologically independent replicates from five individual mice per group. All data are mean ± SEM. Statistics were done by one-way ANOVA followed by adjustments for multiple comparisons.

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