Bierer B E, Peterson A, Barbosa J, Seed B, Burakoff S J
Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115.
Proc Natl Acad Sci U S A. 1988 Feb;85(4):1194-8. doi: 10.1073/pnas.85.4.1194.
To define the role of the CD2-lymphocyte function-associated antigen 3 (LFA-3) interaction in T-cell activation, we have expressed a cDNA encoding the human CD2 molecule in a murine antigen-specific T-cell hybridoma. Expression of the CD2 molecule greatly enhances T-cell responsiveness to antigen; this enhancement is inhibited by anti-CD2 and anti-LFA-3 monoclonal antibodies (mAbs). CD2+ hybridomas produce interleukin 2 in response to combinations of anti-CD2 mAbs 9.6 and 9-1 and, in the presence of mAb 9-1, to sheep erythrocytes or to the LFA-3 antigen. Furthermore, hybridomas expressing a mutant CD2 molecule that has lost mAb 9.6 binding do not exhibit the enhanced response to antigen or the ability to respond to LFA-3 plus mAb 9-1, but these hybridomas retain the ability to respond to combinations of anti-CD2 mAbs. The role of the CD2-LFA-3 interaction in T-cell activation and the potential for other physiologic ligands for CD2 are discussed.
为了确定CD2淋巴细胞功能相关抗原3(LFA-3)相互作用在T细胞激活中的作用,我们在鼠抗原特异性T细胞杂交瘤中表达了编码人CD2分子的cDNA。CD2分子的表达极大地增强了T细胞对抗原的反应性;这种增强被抗CD2和抗LFA-3单克隆抗体(mAb)所抑制。CD2+杂交瘤在抗CD2 mAb 9.6和9-1联合作用下,以及在mAb 9-1存在的情况下,对绵羊红细胞或LFA-3抗原产生白细胞介素2。此外,表达已失去mAb 9.6结合能力的突变型CD2分子的杂交瘤,对抗原的增强反应或对LFA-3加mAb 9-1的反应能力均未表现出来,但这些杂交瘤仍保留了对抗CD2 mAb联合作用的反应能力。本文讨论了CD2-LFA-3相互作用在T细胞激活中的作用以及CD2其他生理配体的可能性。