Wang J, Lenardo M J
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892-1892, USA.
J Exp Med. 1997 Oct 6;186(7):1171-6. doi: 10.1084/jem.186.7.1171.
B cells are susceptible to Fas ligand (FasL)+ CD4(+) Th1 cell-mediated apoptosis. We demonstrate that blocking the interactions between lymphocyte function associated (LFA)-1 and intercellular adhesion molecule(ICAM)-1 and ICAM-2 completely suppresses Fas-dependent B cell lysis. Antibodies to CD2 and CD48 partially suppress B cell apoptosis, whereas anti-B7.1 and anti-B7.2 antibodies have no effect. Also, B cells from ICAM-1-deficient mice are resistant to FasL+ T cell-mediated death. Our results suggest that LFA-1/ICAM interactions are crucial for Th1 cell-mediated B cell apoptosis and may contribute to the maintenance of B cell homeostasis in vivo.
B细胞易受Fas配体(FasL)+ CD4(+)Th1细胞介导的凋亡影响。我们证明,阻断淋巴细胞功能相关抗原-1(LFA-1)与细胞间黏附分子-1(ICAM-1)和ICAM-2之间的相互作用可完全抑制Fas依赖的B细胞裂解。抗CD2和抗CD48抗体可部分抑制B细胞凋亡,而抗B7.1和抗B7.2抗体则无作用。此外,来自ICAM-1缺陷小鼠的B细胞对FasL + T细胞介导的死亡具有抗性。我们的结果表明,LFA-1/ICAM相互作用对于Th1细胞介导的B细胞凋亡至关重要,并且可能有助于体内B细胞稳态的维持。