Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Cell Immunol. 2012 Sep;279(1):66-9. doi: 10.1016/j.cellimm.2012.09.010. Epub 2012 Oct 1.
Cellular immunity is dependent on major histocompatibility complex (MHC) class I molecules enabling cytotoxic T cell recognition of malignant and infected cells. Loading of antigenic peptides onto MHC class I is assisted by a peptide-loading protein complex including tapasin. We found that tapasin expression is enhanced by beta 2-microglobulin via both transcriptional and post-transcriptional mechanisms. In addition, using conditions which preserve the tapasin-ERp57 disulfide-bonded conjugate, we demonstrated that beta 2-microglobulin increases tapasin-containing protein complexes, and reduces the level of MHC class I/ERp57 complexes lacking tapasin. Overall, our results provide a new perspective on the regulation of tapasin expression and association.
细胞免疫依赖于主要组织相容性复合体（MHC）I 类分子，使细胞毒性 T 细胞能够识别恶性和感染细胞。抗原肽加载到 MHC I 类分子上是由包括 tapasin 在内的肽加载蛋白复合物协助的。我们发现β2-微球蛋白通过转录和转录后机制增强 tapasin 的表达。此外，使用保留 tapasin-ERp57 二硫键结合物的条件，我们证明β2-微球蛋白增加了含有 tapasin 的蛋白复合物，并降低了缺乏 tapasin 的 MHC I/ERp57 复合物的水平。总的来说，我们的结果为 tapasin 表达和关联的调节提供了新的视角。
