Moy V T, Brian A A
Department of Chemistry and Cancer Center, University of California, San Diego, La Jolla 92093.
J Exp Med. 1992 Jan 1;175(1):1-7. doi: 10.1084/jem.175.1.1.
To examine the role of lymphocyte function-associated antigen 1 (LFA-1) expression on murine B cells as it pertains to their function in T cell activation, we carried out antigen-presentation assays in tissue culture wells coated with a purified, secreted form of the murine intercellular adhesion molecule 1 (ICAM-1). We observed a significant decrease in the concentration of antigen required to activate a T cell hybridoma and primary T cells in wells coated with ICAM-1. This effect was dependent on the amount of ICAM-1 used to coat the wells and was also observed in wells coated with anti-LFA-1-monoclonal antibodies and was blocked by soluble anti-LFA-1 antibodies. The effect on antigen dose was most pronounced in assays carried out with an ICAM-1-deficient mutant B lymphoma cell line, small resting primary B cells, and unfractionated primary B cells at low concentrations. No decrease in the antigen dose was observed if the B cells were chemically fixed or treated with ricin, or when antigen was presented by a HeLa cell line transfected with murine class II major histocompatibility complex (MHC) genes, indicating that the immobilized ICAM-1 was mediating its effect through B cell LFA-1, and that B cell protein synthesis was required. The enhancing effect was also observed if the B cells were prepulsed with antigen, indicating that improved uptake or processing of antigen, or increased class II MHC expression were unlikely mechanisms.
为了研究淋巴细胞功能相关抗原1（LFA-1）在鼠B细胞上的表达与其在T细胞激活中的功能之间的关系，我们在包被有纯化的、分泌形式的鼠细胞间黏附分子1（ICAM-1）的组织培养孔中进行了抗原呈递试验。我们观察到，在包被有ICAM-1的孔中，激活T细胞杂交瘤和原代T细胞所需的抗原浓度显著降低。这种效应取决于用于包被孔的ICAM-1的量，在用抗LFA-1单克隆抗体包被的孔中也观察到了这种效应，并且被可溶性抗LFA-1抗体阻断。在用ICAM-1缺陷的突变B淋巴瘤细胞系、低浓度的静止原代小B细胞和未分离的原代B细胞进行的试验中，对抗原剂量的影响最为明显。如果B细胞经过化学固定或用蓖麻毒素处理，或者当抗原由转染了鼠II类主要组织相容性复合体（MHC）基因的HeLa细胞系呈递时，未观察到抗原剂量的降低，这表明固定化的ICAM-1是通过B细胞LFA-1介导其效应的，并且需要B细胞蛋白质合成。如果用抗原预脉冲B细胞，也观察到了增强效应，这表明抗原摄取或加工的改善，或II类MHC表达的增加不太可能是其机制。
