Altered antigen presentation in mice lacking H2-O
Altered antigen presentation in mice lacking H2-O
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DOI：
10.1016/s1074-7613(00)80475-6
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发表时间：
1998-02-01
期刊：
影响因子：
32.4
通讯作者：
Karlsson, L
中科院分区：
文献类型：
--
作者：
Liljedahl, M;Winqvist, O;Karlsson, L
HLA-DM催化MHC II类相关的不变链衍生肽（CLIP）从II类分子释放。最近有证据表明，HLA-DO是B细胞中HLA-DM的负调节因子，但其生理功能尚不清楚。对缺乏H2-O（相当于小鼠的HLA-DO）的小鼠B细胞抗原呈递的分析，以及使用纯化的HLA-DO和HLA-DM分子进行的生化分析表明，HLA-DO/H2-O通过限制HLA-DM活性的pH范围来影响II类分子的肽负载。这种作用可能有助于减少由液相内吞作用内化的抗原呈递，从而使B细胞介导的抗原呈递集中于由膜免疫球蛋白内化的抗原。
HLA-DM catalyzes the release of MHC class II-associated invariant chain-derived peptides (CLIP) from class II molecules. Recent evidence has suggested that HLA-DO is a negative regulator of HLA-DM in B cells, but the physiological function of HLA-DO remains unclear. Analysis of antigen presentation by B cells from mice lacking H2-O (the mouse equivalent of HLA-DO), together with biochemical analysis using purified HLA-DO and HLA-DM molecules, suggests that HLA-DO/H2-O influences the peptide loading of class II molecules by limiting the pH range in which HLA-DM is active. This effect may serve to decrease the presentation of antigens internalized by fluid-phase endocytosis, thus concentrating the B cell-mediated antigen presentation to antigens internalized by membrane immunoglobulin.