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- W4313381729 abstract "Abstract Generalized pustular psoriasis (GPP) is a rare inflammatory skin disorder with an etiology distinct from common plaque psoriasis. GPP patients often do not respond to therapeutic agents used routinely to treat plaque psoriasis. Genetic evidence suggests that GPP arises from dysfunction in the IL36/IL36Ra/IL36R signaling axis, and many aspects of GPP can be re-created in the mouse by intradermal (ID) injection of pre-activated IL36. We have used this ID-IL36 model to study the leukocyte populations that accumulate within GPP skin. In a previous study, we reported that a small molecule CCR6 antagonist, CCX2553, ameliorates inflammation in an imiquimod-induced model of plaque psoriasis, and we now find this is to be the case in the GPP model as well. However, in contrast to the imiquimod model, a conventional CD4+ αβ T cell population accumulates in the ID-IL36-treated skin instead of the characteristic γδT17 population found in imiquimod-treated skin. CCX2553 reduces IL36-induced inflammation while preventing skin accumulation of this CD4+ αβT cell population. Thus, although disparate T cell populations are associated with each model, inflammation is ameliorated by CCR6 antagonism in both models. These findings suggest that CCR6 may constitute a novel target for a mechanistically distinct approach towards GPP therapy." @default.
- W4313381729 created "2023-01-06" @default.
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- W4313381729 date "2018-05-01" @default.
- W4313381729 modified "2023-10-18" @default.
- W4313381729 title "IL36-Mediated Skin Inflammation Requires Signaling Through Chemokine Receptor CCR6." @default.
- W4313381729 doi "https://doi.org/10.4049/jimmunol.200.supp.176.19" @default.
- W4313381729 hasPublicationYear "2018" @default.
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