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• W2103257656 abstract "The Bordetella pertussis adenylate cyclase toxin (CyaA) assists infection by potently suppressing the host immune response. Although CyaA effectively targets T lymphocytes, its putative receptor on these cells is unknown. Here, we show that CyaA binds to T cells via the β2 integrin LFA-1 in its active conformation. CyaA clusters with LFA-1 at the immune synapse (IS), from which it induces the premature disengagement of LFA-1 concomitant with the dissipation of talin, which tethers the integrin to the underlying actin cytoskeleton. The CyaA-induced redistribution of LFA-1 was cAMP- and protein kinase A (PKA)–dependent. These results not only identify LFA-1 as a CyaA receptor on T cells but unveil a novel mechanism of immunosuppression whereby the toxin parasitizes its interaction with LFA-1 to inhibit signaling at the IS through the local production of cAMP. The data also provide novel insights into the role of cAMP/PKA signaling in controlling the dynamics of the IS." @default.
• W2103257656 created "2016-06-24" @default.
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• W2103257656 date "2011-05-16" @default.
• W2103257656 modified "2023-10-16" @default.
• W2103257656 title "The <i>Bordetella pertussis</i> adenylate cyclase toxin binds to T cells via LFA-1 and induces its disengagement from the immune synapse" @default.
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• W2103257656 doi "https://doi.org/10.1084/jem.20101558" @default.
• W2103257656 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3173238" @default.
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• W2103257656 hasPublicationYear "2011" @default.
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