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- W4313356641 abstract "Abstract Although it has been previously reported that mice deficient in SOCS1 develop lupus-like pathologies including skin lesions, the contributing pathogenic mechanisms have not been fully elucidated. We have observed that SOCS1+/- IFNγ-/- mice, but not IFNγ-/-, SOCS1+/-, or wild-type mice develop significant spontaneous skin pathology on the back and ears. The hyperplasia was characterized by significant accumulations of CD3+ T cells, F4/80+ macrophages, and neutrophils. Moreover, SOCS1+/- IFNγ-/- mice presented with lymphadenopathy and splenomegaly. Notably, SOCS1+/- IFNγ-/- leukocytes stimulated with αCD3/αCD28 in vitro were hyper proliferative and produced significant amounts of IL17 and IL-6 compared to IFNy-/- controls. To assess the contribution of excess IL17 production in this overt pathology, SOCS1+/- IFNy-/- mice were treated with IL17 neutralizing antibodies or an IgG control. Strikingly, administration of αIL17 mediated a significant reduction in lymphadenopathy, comparable to IFNγ-/- mice. Moreover, αIL17 treatment significantly reduced dermal leukocyte infiltration and skin lesions compared to SOCS1+/- IFNγ-/- mice receiving IgG control or no treatment. Together, these results present a novel role of SOCS1 in the regulation of IL17 production and subsequent onset of spontaneous skin pathology. Furthermore, these data suggest that amelioration of SOCS1 deficiency using SOCS1 mimetic peptides may have implications in the regulation of inflammatory skin pathologies." @default.
- W4313356641 created "2023-01-06" @default.
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- W4313356641 date "2015-05-01" @default.
- W4313356641 modified "2023-09-23" @default.
- W4313356641 title "Aberrant IL-17 production, mediated by SOCS1 deficiency, promotes inflammatory skin pathologies and lymphadenopathy in an IFN gamma independent manner. (THER2P.957)" @default.
- W4313356641 doi "https://doi.org/10.4049/jimmunol.194.supp.67.8" @default.
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