ArticleNature communications2024
Androgens contribute to sex bias of autoimmunity in mice by T cell-intrinsic regulation of Ptpn22 phosphatase expression.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Reduced Tumor Control in Males Can Result from Impaired CD4+ T-cell Help through the CD40L-CD40 Pathway.Cancer immunology research · 2026Article
- Heterogeneity in the association of genetic risk for RA and resultant RA phenotypes.Rheumatology (Oxford, England) · 2026Article
- Inflammatory bowel disease and prostate cancer: from epidemiological controversy to mechanistic hypotheses.Frontiers in immunology · 2026Review
- Is the NOD mouse a good model for type 1 diabetes?Diabetologia · 2026Review
- Sex bias in tumor immunity: insights from immune cells.Theranostics · 2025Review
- Protein phosphatases in systemic autoimmunity.Immunometabolism (Cobham, Surrey) · 2025Review
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Authors and funding
9 authors.
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Abstract
Autoimmune diseases such as systemic lupus erythematosus (SLE) display a strong female bias. Although sex hormones have been associated with protecting males from autoimmunity, the molecular mechanisms are incompletely understood. Here we report that androgen receptor (AR) expressed in T cells regulates genes involved in T cell activation directly, or indirectly via controlling other transcription factors. T cell-specific deletion of AR in mice leads to T cell activation and enhanced autoimmunity in male mice. Mechanistically, Ptpn22, a phosphatase and negative regulator of T cell receptor signaling, is downregulated in AR-deficient T cells. Moreover, a conserved androgen-response element is found in the regulatory region of Ptpn22 gene, and the mutation of this transcription element in non-obese diabetic mice increases the incidence of spontaneous and inducible diabetes in male mice. Lastly, Ptpn22 deficiency increases the disease severity of male mice in a mouse model of SLE. Our results thus implicate AR-regulated genes such as PTPN22 as potential therapeutic targets for autoimmune diseases.
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