Mazerolles F, Lumbroso C, Lecomte O, Le Deist F, Fischer A
INSERM U 132, Hôpital des Enfants Malades, Paris, France.
Eur J Immunol. 1988 Aug;18(8):1229-34. doi: 10.1002/eji.1830180813.
The functional role of the LFA-1 molecule in the interaction between helper T lymphocytes and B lymphocytes was investigated using lymphocytes from patients with leukocyte adhesion deficiency, an inherited immunodeficiency characterized by a defective leukocyte expression of the LFA-1, Mac-1 (CR3) and p150,95 molecules. The ability of LFA-1- T lymphocytes to provide antigen-specific help for HLA-identical LFA-1+ B lymphocytes was reduced while their antigen-specific activation was normal. Antigen-independent conjugate formation between resting, nonactivated LFA-1- T lymphocytes and LFA-1+ B lymphocytes was impaired while LFA-1- B lymphocytes bound LFA-1+ T lymphocytes normally. Conjugate formation of activated LFA-1- T lymphocytes was mostly mediated by the CD2-LFA-3 adhesion pathway while the ICAM-1 molecule, a ligand of LFA-1, had no function. These results demonstrate that LFA-1 plays a major role in the cognate interaction between helper T lymphocytes and B lymphocytes that cannot be mediated instead by CD2 or other molecules on resting T lymphocytes.
利用来自白细胞黏附缺陷患者的淋巴细胞,对淋巴细胞功能相关抗原-1(LFA-1)分子在辅助性T淋巴细胞与B淋巴细胞相互作用中的作用进行了研究。白细胞黏附缺陷是一种遗传性免疫缺陷病,其特征为LFA-1、巨噬细胞抗原-1(CR3)和p150,95分子的白细胞表达存在缺陷。LFA-1缺陷的T淋巴细胞为人类白细胞抗原(HLA)相同的LFA-1阳性B淋巴细胞提供抗原特异性辅助的能力降低,而其抗原特异性激活正常。静息、未激活的LFA-1缺陷T淋巴细胞与LFA-1阳性B淋巴细胞之间不依赖抗原的共轭形成受损,而LFA-1缺陷的B淋巴细胞与LFA-1阳性T淋巴细胞的结合正常。激活的LFA-1缺陷T淋巴细胞的共轭形成主要由CD2-LFA-3黏附途径介导,而LFA-1的配体细胞间黏附分子-1(ICAM-1)分子则无功能。这些结果表明,LFA-1在辅助性T淋巴细胞与B淋巴细胞的同源相互作用中起主要作用,而静息T淋巴细胞上的CD2或其他分子无法替代其介导这种相互作用。