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• W3205647387 abstract "Abstract Immune checkpoint inhibitor (ICI) therapies that promote T cell activation have improved outcomes for advanced malignancies yet also elicit harmful autoimmune reactions. The T cell mechanisms mediating these iatrogenic autoimmune events remain unclear. Here we assayed T cells from joints of patients affected by ICI-induced inflammatory arthritis (ICI-arthritis), which can present clinically indistinguishable from rheumatoid arthritis (RA). Compared to the autoimmune arthritides RA and psoriatic arthritis (PsA), ICI-arthritis joints contained an expanded CD38 hi CD127 − CD8 + T cell subset that displays cytotoxic, effector, and interferon (IFN) response signatures. The abundance of CD38 hi CD8 T cells in ICI-arthritis resulted from a limited number of clones that could be found proliferating in the joint. Exposure of synovial T cells to Type I IFN, more so than IFN-γ, induces the CD38 hi cytotoxic phenotype. Relative to other CD8 + T cell subsets in the joints, the CD38 hi population is distinct from a dysfunctional population and clonally most related to TCF7 + memory populations. Examination of synovial tissue from bilateral knee arthroplasty demonstrated considerable sharing of TCR clonotypes in the CD38 hi CD8 T cell fraction from both knees. These results define a distinct CD8 T cell subset that may be directly activated by ICI therapy and mediate a tissue-specific autoimmune cellular reaction in patient joints." @default.
• W3205647387 created "2021-10-25" @default.
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• W3205647387 date "2021-10-20" @default.
• W3205647387 modified "2023-10-16" @default.
• W3205647387 title "Clonally expanded CD38^hi cytotoxic CD8 T cells define the T cell infiltrate in checkpoint inhibitor-associated arthritis" @default.
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• W3205647387 doi "https://doi.org/10.1101/2021.10.19.464961" @default.
• W3205647387 hasPublicationYear "2021" @default.
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