Plasma phospholipid transfer protein (PLTP) modulates adaptive immune functions through alternation of T helper cell polarization.
Fiche publication
Date publication
novembre 2016
Journal
Cellular & molecular immunology
Auteurs
Membres identifiés du Cancéropôle Est :
Dr LAGROST Laurent, Dr SEQUEIRA-LEGRAND Anabelle, Dr PAIS DE BARROS Jean-Paul, Pr KAHN Naim
Tous les auteurs :
Desrumaux C, Lemaire-Ewing S, Ogier N, Yessoufou A, Hammann A, Sequeira-Le Grand A, Deckert V, Pais de Barros JP, Le Guern N, Guy J, Khan NA, Lagrost L
Lien Pubmed
Résumé
Plasma phospholipid transfer protein (PLTP) is a key determinant of lipoprotein metabolism, and both animal and human studies converge to indicate that PLTP promotes atherogenesis and its thromboembolic complications. Moreover, it has recently been reported that PLTP modulates inflammation and immune responses. Although earlier studies from our group demonstrated that PLTP can modify macrophage activation, the implication of PLTP in the modulation of T-cell-mediated immune responses has never been investigated and was therefore addressed in the present study. Approach and results: In the present study, we demonstrated that PLTP deficiency in mice has a profound effect on CD4(+) Th0 cell polarization, with a shift towards the anti-inflammatory Th2 phenotype under both normal and pathological conditions. In a model of contact hypersensitivity, a significantly impaired response to skin sensitization with the hapten-2,4-dinitrofluorobenzene (DNFB) was observed in PLTP-deficient mice compared to wild-type (WT) mice. Interestingly, PLTP deficiency in mice exerted no effect on the counts of total white blood cells, lymphocytes, granulocytes, or monocytes in the peripheral blood. Moreover, PLTP deficiency did not modify the amounts of CD4(+) and CD8(+) T lymphocyte subsets. However, PLTP-deficiency, associated with upregulation of the Th2 phenotype, was accompanied by a significant decrease in the production of the pro-Th1 cytokine interleukin 18 by accessory cells.
Référence
Cell. Mol. Immunol.. 2016 Nov;13(6):795-804