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© 1993 Oxford University Press

research-article

Effects of 7,12-Dimethylbenz[a]anthracene on the Superantigen Toxic Shock Syndrome Toxin (TSST-1)-Induced Proliferation and Antibody Secretion by Human Lymphocytes1

STEVEN C. WOOD and MICHAEL P. HOLSAPPLE2

Department of Pharmacology and Toxicology, Medical College of Virginia, Virginia Commonwealth University Box 613, MCV Station, Richmond, Virginia 23298

Received June 25, 1992; accepted December 21, 1992

Toxic shock syndrome toxin (TSST-1), a 22-kDa exotoxin secreted by Staphylococcus aureus, can act as a nominal antigen and induce proliferation and immunoglobulin secretion in human B-cells. The purpose of the present studies was to examine the effect of 7,12-dimethylbenz[a]anthracene (DMBA), a well-characterized immunosuppressant of both cell-mediated and humoral immunity in murine lymphocytes, upon the mixed lymphocyte reaction (MLR) and TSST-1-induced immune responses in human lymphocytes. The MLR, using human tonsillar lymphocytes (HTL) from four different donors, was inhibited in a dose-dependent manner from 1 to 100 µM. The IC50 for the suppression of the MLR ranged from 10 to 40 µM. TSST-1 is a potent stimulator of T-cells bearing specific VB regions on the T-cell receptor (TCR). In contrast with the results from the MLR, DMBA inhibited TSST-1-induced T-cell proliferation only at 100 µM in HTL. A similar profile of activity was determined with splenic T-cells from a single donor. TSST-1 has also been demonstrated to induce specific B-cell proliferation and differentiation in the presence of irradiated T-cells. TSST-1-induced B-cell proliferation was only consistently and markedly inhibited by DMBA at 100 µM in tonsillar and splenic lymphocytes. In contrast, TSST-1-induced B-cell differentiation, as manifested by IgM and IgG secretion, was inhibited in a dose-dependent manner from 1 to 100 µM DMBA in B-cells from human tonsils and spleens. These preliminary results suggest that TSST-1-induced immunoglobulin secretion may be a powerful model for the study of the modulation of human B-cell effector function by xenobiotics in vitro.


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