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Such regulatory dynamics parallel those attributed to deubiquitinating enzymes, suggesting that USP17L26 may similarly modulate protein turnover in these pathways."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "14"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond controlling kinase cascades, USP17L26 may also influence the immune microenvironment by modulating chemokine signals. Several abstracts underscore the role of the CCL22–CCR4 axis in recruiting regulatory T cells and shaping both innate and adaptive immune responses in contexts ranging from autoimmune diabetes to inflammatory bone resorption and tumor immunosuppression. 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