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- W2019310318 abstract "Autoreactive memory T lymphocytes are implicated in the pathogenesis of autoimmune diseases. Here we demonstrate that disease-associated autoreactive T cells from patients with type-1 diabetes mellitus or rheumatoid arthritis (RA) are mainly CD4 + CCR7 − CD45RA − effector memory T cells (T EM cells) with elevated Kv1.3 potassium channel expression. In contrast, T cells with other antigen specificities from these patients, or autoreactive T cells from healthy individuals and disease controls, express low levels of Kv1.3 and are predominantly naïve or central-memory (T CM ) cells. In T EM cells, Kv1.3 traffics to the immunological synapse during antigen presentation where it colocalizes with Kvβ2, SAP97, ZIP, p56 lck , and CD4. Although Kv1.3 inhibitors [ShK(L5)-amide (SL5) and PAP1] do not prevent immunological synapse formation, they suppress Ca 2+ -signaling, cytokine production, and proliferation of autoantigen-specific T EM cells at pharmacologically relevant concentrations while sparing other classes of T cells. Kv1.3 inhibitors ameliorate pristane-induced arthritis in rats and reduce the incidence of experimental autoimmune diabetes in diabetes-prone (DP-BB/W) rats. Repeated dosing with Kv1.3 inhibitors in rats has not revealed systemic toxicity. Further development of Kv1.3 blockers for autoimmune disease therapy is warranted." @default.
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- W2019310318 date "2006-11-14" @default.
- W2019310318 modified "2023-10-11" @default.
- W2019310318 title "Kv1.3 channels are a therapeutic target for T cell-mediated autoimmune diseases" @default.
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- W2019310318 doi "https://doi.org/10.1073/pnas.0605136103" @default.
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