Of self-lipids, CD1-restricted T cells, and contact sensitization

Contact hypersensitivity (CHS) in rodents and contact dermatitis in humans are long-known pathological conditions caused by MHC-restricted T-cell responses. These responses are triggered upon T-cell recognition of neo-antigenic determinants, which are generated by a variety of environmental contact sensitizer (CS) chemicals associating with self-proteins to comprise these neo-antigens. In this issue of the European Journal of Immunology, Betts et al. [Eur. J. Immunol. 2017. 47: 1171–1180] provide intriguing data implying that common small molecule CSs such as dinitrochlorobenzene can also recruit and activate autoreactive CD1-restricted T cells specific for cell-endogenous lipids, which are enriched in human skin. The effects of dinitrochlorobenzene on CD1 T-cell recruitment and function were dependent on newly synthesized CD1 molecules and the presence of endogenous lipids. These findings shed new light on unanticipated mechanisms that have potential clinical relevance on a common and highly distressing disease state.

Small contact sensitizers (CSs) xenobiotics such as dinitrochlorobenzene cause contact dermatitis via self-protein modification and MHC-restricted T-cell activation. Their sensitizing mechanisms seem much wider as it is now shown that CSs can also activate autoreactive CD1-restricted T cells specific for cell-endogenous lipids, which are enriched in human skin.

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