Zhou X, Glas R, Liu T, Ljunggren H G, Jondal M
Department of Immunology, Karolinska Institute, Stockholm, Sweden.
Eur J Immunol. 1993 Aug;23(8):1802-8. doi: 10.1002/eji.1830230811.
Cytotoxic T lymphocytes (CTL) recognize foreign antigens as short peptides presented by class I molecules of the major histocompatibility complex (MHC). T2 cells are profoundly defective in the presentation of endogenously synthesized antigens to CTL due to a deletion of MHC class II-encoded genes for transporters associated with antigen presentation (TAP1/TAP2). Surprisingly, we here demonstrate that T2 cells, after infection with Sendai virus, are readily killed by H-2Kb restricted CD8+ T cells. In contrast to classical class I-mediated antigen presentation, the presentation of Sendai virus antigen in T2Kb cells is brefeldin A (BFA) insensitive. The present findings may suggest the presence of an alternative pathway for MHC class I-mediated antigen presentation in T2 cells.
细胞毒性T淋巴细胞（CTL）将外来抗原识别为主要组织相容性复合体（MHC）I类分子呈递的短肽。由于与抗原呈递相关的转运体（TAP1/TAP2）的MHC II类编码基因缺失，T2细胞在内源性合成抗原呈递给CTL方面存在严重缺陷。令人惊讶的是，我们在此证明，仙台病毒感染后的T2细胞很容易被H-2Kb限制性CD8 + T细胞杀死。与经典的I类介导的抗原呈递不同，T2Kb细胞中仙台病毒抗原的呈递对布雷菲德菌素A（BFA）不敏感。目前的研究结果可能表明T2细胞中存在MHC I类介导的抗原呈递的替代途径。
