Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA.
PLoS One. 2013 Aug 29;8(8):e72867. doi: 10.1371/journal.pone.0072867. eCollection 2013.
CD1d molecules are structurally similar to MHC class I, but present lipid antigens as opposed to peptides. Here, we show that MHC class I molecules physically associate with (and regulate the functional expression of) mouse CD1d on the surface of cells. Low pH (3.0) acid stripping of MHC class I molecules resulted in increased surface expression of murine CD1d on antigen presenting cells as well as augmented CD1d-mediated antigen presentation to NKT cells. Consistent with the above results, TAP1-/- mice were found to have a higher percentage of type I NKT cells as compared to wild type mice. Moreover, bone marrow-derived dendritic cells from TAP1-/- mice showed increased antigen presentation by CD1d compared to wild type mice. Together, these results suggest that MHC class I molecules can regulate NKT cell function, in part, by masking CD1d.
CD1d 分子在结构上与 MHC I 类分子相似,但作为配体的是脂质抗原,而不是肽。在这里,我们发现 MHC I 类分子在细胞表面与(并调节)小鼠 CD1d 的功能表达发生物理关联。低 pH(3.0)酸性剥离 MHC I 类分子导致抗原呈递细胞表面的鼠 CD1d 表达增加,并且 CD1d 介导的对 NKT 细胞的抗原呈递增加。与上述结果一致,与野生型小鼠相比,TAP1-/- 小鼠被发现具有更高比例的 I 型 NKT 细胞。此外,TAP1-/- 小鼠的骨髓来源树突状细胞通过 CD1d 呈递的抗原比野生型小鼠增加。综上所述,这些结果表明 MHC I 类分子可以通过遮蔽 CD1d 来调节 NKT 细胞的功能。