ArticleJCI insight2025
Deletion of Ptpn2 in B cells promotes autoimmunity via TLR and JAK/STAT signaling.
Article in JCI insight, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Review
- Activation of Anergic B Cells During Development of Autoimmunity.Immunological reviews · 2026Review
- Ptpn2 limits plasma cell fate and antiviral immunity by integrating B cell receptor and IFN-γ signals in B cells.Science advances · 2026Article
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Authors and funding
9 authors.
Funding
Abstract
Autoimmunity arises when self-reactive B and T cells target the body's own tissues, with B cells contributing through antigen presentation as well as production of autoantibodies and proinflammatory cytokines. Genome wide association studies (GWAS) and recent identification of loss-of-function gene variants in individuals with young-onset autoimmunity have highlighted a role for protein tyrosine phosphatase nonreceptor type 2 (PTPN2) in development of autoimmunity. While prior studies have focused on the mechanism of Ptpn2 in T cells and other cell types, its function in B cells has not been explored. To test the B cell-intrinsic roles of Ptpn2, we generated a B cell-specific deletion of Ptpn2 in mice (Mb1-Cre;Ptpn2fl/fl). We found that loss of Ptpn2 in B cells promoted organ inflammation, increased the frequency of age/autoimmune-associated B cells (ABCs) and plasmablasts in the periphery, and increased circulating autoantibodies. Moreover, we found that Ptpn2 acted as a negative regulator of the JAK/STAT and TLR7 pathways in B cells. In line with this, treatment of B cells from Mb1-Cre;Ptpn2fl/fl mice with IFN-γ and TLR7 agonist lead to enhanced differentiation into ABCs. These findings highlight the critical roles of Ptpn2 in B cell function and its potential as a key regulator in preventing B cell associated autoimmunity.
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Registered trials
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