Aichinger G, Lechler R I
Department of Immunology, RPMS, Hammersmith Hospital, London, U.K.
Biochem Soc Trans. 1995 Aug;23(3):657-60. doi: 10.1042/bst0230657.
Assembly, targeting and peptide loading of MHC class II molecules is controlled by a series of mechanisms and molecular interactions that inhibit the binding of peptides or proteins in the ER or secretory compartment. As a consequence, the major site of peptide binding to class II molecules is in the endosomal/lysosomal compartment. The barrier, however, between exogenous and endogenous antigen presentation by MHC class II molecules does not seem to be as tight as for MHC class I, and several different mechanisms may contribute to MHC class II presentation of endogenous antigens. Although limited, the possibility of presentation of endogenous antigens may nevertheless be important in viral infections and in tumours, for the recruitment of CD4-positive helper T-cells. This may also apply when unfolded or misfolded proteins accumulate in the ER and compete with the invariant chain for binding to MHC class II molecules. The potential relevance of this pathway to triggering autoimmune reactions has yet to be explored.
MHC II类分子的组装、靶向和肽装载受一系列机制和分子相互作用的控制，这些机制和相互作用会抑制肽或蛋白质在ER或分泌区室中的结合。因此，肽与II类分子结合的主要部位是在内体/溶酶体区室。然而，MHC II类分子对外源和内源性抗原呈递的屏障似乎不像MHC I类那样紧密，几种不同的机制可能有助于MHC II类对内源性抗原的呈递。尽管可能性有限，但内源性抗原呈递在病毒感染和肿瘤中对于招募CD4阳性辅助性T细胞可能仍然很重要。当未折叠或错误折叠的蛋白质在ER中积累并与恒定链竞争结合MHC II类分子时，情况可能也是如此。这条途径与引发自身免疫反应的潜在相关性还有待探索。
