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The Journal of Immunology, Vol 146, Issue 5 1422-1427, Copyright © 1991 by American Association of Immunologists
ARTICLES |
S Murakami, K Miyake, R Abe, PW Kincade and RJ Hodes
Experimental Immunology Branch, National Cancer Institute, NIH, Bethesda, MD 20892.
This study was undertaken to identify and isolate the pathophysiologically important B cell subpopulation which is activated to Ig secretion and autoantibody production in stimulatory (chronic) graft-vs-host (GVH) reactions. We recently demonstrated that IL-5 stimulation in vitro induces the appearance of a distinct CD44hi Ialow CD45Rlow B cell subpopulation that has aquired the ability to bind to hyaluronate (HA), one of the ligands for CD44, and that this B cell subpopulation is enriched in both proliferative and Ig-secretory responses. In the present report, CD44 expression was examined in B cells which were activated in the course of stimulatory GVH reactions. Compared with normal mice, B cells from mice undergoing stimulatory GVH reactions contained a novel CD44hi B cell subpopulation which exhibited enhanced binding to HA. The CD44hi HA-adherent B cell subpopulation from GVH mice spontaneously secreted large amounts of Ig, particularly IgG, including autoantibody specific for ssDNA. These findings demonstrate that CD44 expression distinguishes those B cells that are activated in vivo in the course of GVH to proliferate and differentiate into Ig-secreting cells. These CD44hi, HA-adherent, cells may play a prominent role in the hypergammaglobulinemia and immune complex glomerulonephritis that occur during chronic GVH reactions.
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