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Alternative splicing is one of the mechanisms which drives diversification of innate immune responses. Spliced isoforms of Toll-interacting protein (Tollip), a negative regulator of TLR2-, TLR4- and IL-1R-induced signalling, have been identified to express at endogenous level in human and mouse macrophages. In the current study, we focused on two Tollip isoforms, the full-length Tollip.a and a mouse-specific isoform Tollip.b that lacks the ubiquitin-binding CUE domain. We asked for the effectsdoi:10.25904/1912/891 fatcat:fyyfpyqurnhlvlr72iazr4vu44