Levine S, Xian C Y, Agocha B, Allopenna J, Welte K, Armstrong D, Yang S Y, Evans R L
Memorial Sloan-Kettering Cancer Center, New York, New York.
Cell Immunol. 1991 Feb;132(2):366-76. doi: 10.1016/0008-8749(91)90034-9.
MAb anti-Leu-13 reacts with a 16-kDa-interferon-responsive lymphocyte-endothelial cell surface antigen and has been demonstrated to induce lymphocyte aggregation by an undefined adhesion pathway. While anti-Leu-13 inhibits proliferation triggered by CD3 antibodies it was found to consistently augment proliferation induced by a pair of CD2 antibodies at suboptimally mitogenic concentrations. The latter mechanism of T cell activation may represent an antigen-nonspecific activation pathway requiring extensive cell-cell interaction. Proliferation induced via the CD2 pathway was very sensitive to the presence of monocytes whose inhibitory effect was reversed by indomethacin. While the potent inhibitory effect of PGE2 on proliferation induced via the CD2 pathway was weakly antagonized by anti-Leu-13, the combined effects of anti-Leu-13 and PGE2 on the CD3 pathway were additive and very inhibitory. The possibility that the Leu-13 signal reflects a mechanism by which a monocyte/macrophage-sensitive T cell activation pathway might be selectively amplified in vivo is discussed.
抗Leu-13单克隆抗体与一种16 kDa的干扰素反应性淋巴细胞-内皮细胞表面抗原发生反应,并且已被证明可通过一种不明的黏附途径诱导淋巴细胞聚集。虽然抗Leu-13抑制由CD3抗体触发的增殖,但发现在亚最佳促有丝分裂浓度下,它能持续增强由一对CD2抗体诱导的增殖。T细胞激活的后一种机制可能代表一种需要广泛细胞间相互作用的抗原非特异性激活途径。通过CD2途径诱导的增殖对单核细胞的存在非常敏感,其抑制作用可被消炎痛逆转。虽然PGE2对通过CD2途径诱导的增殖的强大抑制作用被抗Leu-13轻微拮抗,但抗Leu-13和PGE2对CD3途径的联合作用是相加的且具有很强的抑制性。讨论了Leu-13信号反映单核细胞/巨噬细胞敏感的T细胞激活途径可能在体内被选择性放大的机制的可能性。