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- W2334846875 abstract "Multiple sclerosis (MS) is associated with impaired function of regulatory immune cell subsets. A new immunoregulatory role for human CD56bright NK cells (CD56brNK) recently emerged, with in vitro demonstration that activation of NK cells with IL-27, IL-2 or anti-CD25 antibody induces suppressor function of CD56br NK toward autologous T cells with mechanisms not fully explained. IL-12, over expressed by antigen-presenting cells in MS, also induces activation of NK cells and their expression of cytokines in vitro, in combination with IL-15. We therefore hypothesize that upon IL-12/IL-15 stimulation, CD56brNK acquire T-cell suppressor function to regulate T-cell activation in inflammatory conditions. Through proliferation assay of CD3/CD28-stimulated T cells, we found that exposure to IL-12/IL-15 for 3 days induces a suppressor function of CD56brNK towards activated, but not resting, autologous CD4+ T cells. We postulated that killing was part of the suppressive mechanism, likely attributable to Granzyme B whose mRNA expression was selectively induced in stimulated CD56brNK. Using a FACS-based assay, we found that stimulated CD56brNK are able to kill autologous activated CD4+ T cells directly through degranulation. In order to assess which NK receptor(s) could be involved in T-cell suppression, we analyzed the proliferation of T cells co-cultured with CD56brNK in the presence of blocking NK receptor antibodies. We found that the selective inhibition of Natural Cytotoxicity Receptors (NCR: NKp30, NKp44, NKp46), but not other tested receptors, restored CD4+ T cell proliferation, suggesting that these receptors are primarily involved in CD56brNK immunoregulatory function. Taken together, these data, provide insights for the mechanism by which the CD56brNK regulate the activation of autologous CD4+ T cells. We investigated CD56brNK in patients with MS to determine whether or not this regulatory cell subset is impaired in MS. We could not detect differences in the proportion of CD56brNK; however, we observed that CD56brNK from MS patients are less able to suppress the proliferation of autologous CD4+ T cells and are apparently impaired in their expression of NCR." @default.
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- W2334846875 date "2014-10-01" @default.
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- W2334846875 title "Unraveling the regulatory role of NK cells on T-cell effector functions: Implications for CNS autoimmunity" @default.
- W2334846875 doi "https://doi.org/10.1016/j.jneuroim.2014.08.144" @default.
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