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Department of Microbiology and Immunology, University of Illinois at the Medical Center, Chicago, Illinois 60612
Abstract
We have adapted an in vitro culture system to study the dose-dependent effects of purified anti-light chain allotype (b4 or b5) antibody on the primary Ab response of rabbit spleen cells to sheep erythrocytes. At high doses, anti-b4 or anti-b5 Ab suppressed the anti-SRBC response and the expression of cell surface immunoglobulins while stimulating blastogenesis and thymidine incorporation. At low doses, anti-allotype Ab markedly enhanced the immune response and, to a lesser extent, thymidine incorporation and blastogenesis. The mitogenic effect of anti-allotype Ab was observed in the absence of antigen only at the higher doses. When tested on heterozygous b4b5 SpC, the high and low doses of Ab selectively modulated the immune response with respect to cells bearing the target allotype. In vivo induced allotype suppression could not be reversed by culturing SpC with high or low doses of purified anti-allotype Ab directed against the expressed allotype. Our data support the concept that anti-Ig Ab reacts directly with B cell surface Ig to trigger a mitogenic response. This trigger, however, is not sufficient to induce differentiation to anti-SRBC secreting cells in the absence of the antigen.
Footnotes
1 This work was supported by Research Grants PHS AI-07043 and CA-05110.
2 Presented in part as an abstract at the 62nd annual meeting of the Federation of American Societies for Experimental Biology, Atlanta, Georgia, June, 1978.
3 Recipient of National Research Fellowship Award (National Institutes of Health). Present address: Institute of Molecular Biophysics, Florida State University, Tallahassee, Florida 32306.
4 In partial fulfillment of the requirements for the Doctor of Philosophy degree in the Graduate College, University of Illinois at the Medical Center, Chicago, Illinois 60612. Present address: Department of Bacteriology, University of California at Los Angeles, Los Angeles, California 90024.
5 To whom reprint requests should be addressed.
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