The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1997/10/1171/ $5.00
The Journal of Experimental Medicine, Volume 186, Number 7, October 6, 1997 1171-1176

Brief Definitive Reports

Essential Lymphocyte Function Associated 1 (LFA-1): Intercellular Adhesion Molecule Interactions for T Cell–mediated B Cell Apoptosis by Fas/APO-1/CD95

Jin Wang and Michael J. Lenardo

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.

Address correspondence to Michael J. Lenardo, Laboratory of Immunology, NIAID, NIH, Bldg 10, RM 11D09, 10 Center Drive MSC 1892, Bethesda, MD 20892-1892. Phone: 301-496-6754; FAX: 301-496-0222; E-mail: lenardo{at}nih.gov

J. Wang was supported by a Fellowship from the Arthritis Foundation.


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