Kim Min Kyung, Choi Yoon-La, Kim Min Kyung, Kim Seok-Hyung, Choi Eun Young, Park Won Seo, Bae Young Mee, Woo Sang Kyu, Park Seong Hoe
Department of Pathology, College of Medicine, Seoul National University, Yongun-dong 28, Chongro-gu, Seoul 110-799, South Korea.
FEBS Lett. 2003 Jul 10;546(2-3):379-84. doi: 10.1016/s0014-5793(03)00567-2.
Major histocompatibility complex (MHC) class II surface levels on thymocytes increase after CD99 ligation. The functional implication of the up-regulated MHC class II was assessed by engaging MHC class II on CD99-ligated cells. MHC class II engagement down-modulated surface levels of T cell receptor and MHC molecules, and inhibited apoptosis of CD99-ligated thymocytes and CEM tumor cells, antagonistic effects on the previously reported CD99 functions. The results were reproducible regardless of the order of ligation of MHC class II and CD99. We suggest that signaling via MHC class II on CD99-engaged cells might be involved in the thymic maturation process by damping CD99 ligation effects.
CD99 连接后，胸腺细胞表面的主要组织相容性复合体（MHC）II 类分子水平会升高。通过使 CD99 连接细胞上的 MHC II 类分子相互作用，评估上调的 MHC II 类分子的功能意义。MHC II 类分子相互作用下调了 T 细胞受体和 MHC 分子的表面水平，并抑制了 CD99 连接的胸腺细胞和 CEM 肿瘤细胞的凋亡，这与先前报道的 CD99 功能具有拮抗作用。无论 MHC II 类分子和 CD99 的连接顺序如何，结果都是可重复的。我们认为，CD99 结合细胞上通过 MHC II 类分子发出的信号可能通过减弱 CD99 连接效应而参与胸腺成熟过程。
