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Antibodies to HLA Class I  1 Domain Trigger Apoptosis of CD40-Activated Human B Lymphocytes
Laurent Genestier,
Geneviève Meffre,
Pierre Garrone,
Jean-Jacques Pin,
Yong-Jun Liu,
Jacques Banchereau, and
Jean-Pierre Revillard
From the Laboratory of Immunology, INSERM U80 UCBL, Hôpital E. Herriot, Lyon, France; and Schering-Plough Laboratory for Immunological Research, Dardilly, France.
We analyzed herein whether antibodies to HLA class I  1 domain, which trigger apoptosis of activated T cells, may also control the growth/survival of human B lymphocytes. Addition of monoclonal antibody (MoAb) 90 (mouse IgG1) or YTH862 (rat IgG2b) was found to strongly inhibit the proliferation of CD40-activated total tonsil B cells as well as that of purified naive, germinal center, and memory B-cell subsets. This inhibitory effect was not prevented by addition of B-cell tropic factors, such as interleukin-2 (IL-2), IL-4, and IL-10, and was a result of induced B-cell apoptosis as shown by using a TUNEL assay and DNA electrophoresis. In contrast, engagement of another epitope of the 1 domain, as well as that of the 2 and 3 domains by specific anti-HLA class I MoAbs, failed to inhibit DNA synthesis and to induce apoptosis of CD40-activated B cells. As recently reported for acquisition of sensitivity to Fas (APO-1/CD95) -dependent apoptosis, susceptibility to MoAb90-and YTH862-induced death was restricted to CD40-activated B cells, because resting and anti-IgM-activated B cells did not undergo apoptosis after HLA class I engagement. Moreover, ligation of the B-cell receptor protected CD40-activated B cells from both HLA class I- and Fas-mediated growth inhibition and apoptosis. Taken together, these results show that engagement of the 1 domain of HLA class I induces apoptotic cell death of CD40-activated, but not of antigen-activated B cells, and would, therefore, suggest a possible role for HLA class I molecules in the control of B-cell homeostasis.
Blood, Vol. 90 No. 2 (July 15), 1997:
pp. 726-735
© 1997 by The American Society of Hematology.
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