These studies were carried out to investigate the potential helper T cell repertoire specific for the random copolymer poly(L-Glu55,L-Ala35, L-Phe9)n(GL phi 9) of responder, nonresponder, and (responder x nonresponder)F1 murine strains. We tested the ability of these T cells to collaborate with dinitrophenyl (DNP)-specific primary and secondary B lymphocytes of each strain in response to the antigen CNP-GL phi 9 in the splenic-fragment culture system. The results of these experiments show that there are GL phi 9-specific T lymphocytes in the responder, nonresponder, and F1 strains; but that these three GL phi 9-specific T cell populations differ in their collaborative potential. Responder T cells are able to collaborate with their own syngeneic responder B cells as well as the allogeneic nonresponder B cells in a syngeneic fashion. The F1 T cell population resembles that of the nonresponder in its ability to collaborate with only responder B cells in a syngeneic fashion. Analysis carried out using appropriately selected mouse strains indicate that these results are unlikely to be a result of positive or negative allogeneic effects. The results obtained suggest that individuals within a given murine strain do possess the capacity to collaborate in a syngeneic fashion with B cells of any other MHC-allogeneic strain as well as their own MHC-identical B cells. The nonresponder status in the response to GL phi 9 appears to be the result of a deletion of T cells capable of recognizing antigen in the context of B cells of the nonresponder haplotype. Thus, the MHC gene products appear to play a determinative role in shaping the expressed helper T cell specificity repertoire within an individual mouse strain.
Role of the major histocompatibility gene products in regulating the antibody response to dinitrophenylated poly(L-Glu55,L-Ala35,L-Phe9)n.
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S K Pierce, N R Klinman, P H Maurer, C F Merryman; Role of the major histocompatibility gene products in regulating the antibody response to dinitrophenylated poly(L-Glu55,L-Ala35,L-Phe9)n.. J Exp Med 1 August 1980; 152 (2): 336–349. doi: https://doi.org/10.1084/jem.152.2.336
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