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From the Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National
Institutes of Health, Bethesda, Maryland 20892-1892
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.
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