ARTICLES

Earlier studies from our laboratory demonstrated that the terpolymer of L-glutamic acid, L-alanine, and L-tyrpsine (GAT) stimulated the development of T cells capable of specifically suppressing the antibody responses in vivo and in vitro of nonresponder strains (bearing the H-2(s), H-2(q), and H-2(p) haplotypes) to GAT complexed with an immunogenic carrier, methylated bovine serum albumin, MBSA (1,2). We then extended these findings to another antigen, the copolymer of L-glutamic acid and L-tyrosine (GT). None of 19 inbred or congenic resistant mouse strains developed antibody responses to GT after immunization with this synthetic polypeptide in adjuvants. All the strains investigated, however, developed IgG plaque-forming cells (PFC) primary responses to GT complexed with MBSA (3). This permitted us to determine that: (a) preimmunization with GT suppressed the response to GT-MBSA in certain but not in all strains; (b) the suppression could be transferred by thymocytes and spleen cells from GT-primed animals; (c) the development of GT-specific suppressor cells is under dominant control of H-2- linked gene(s) which have been designated specific immune suppressor genes (Is genes); (d) the Is genes are antigen specific since GAT-MBSA responses are suppressed by GAT in strains carrying the H-2(q) haplotype, while GT-MBSA responses are not suppressed by the related polymer GT in these same strains (3,4).

The experiments reported in this study map the Is genes responsible for GT-specific suppression within the H-2 complex. The data indicate that the K and D loci are not concerned with GT-specific suppression, and that this phenomenon is controlled by complementing or interacting genes which map on either side of cross-over events between the IB and IC subregions.
CiteULike    Complore    Connotea    Del.icio.us    Digg    Facebook    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

• Hattori, M, Buse, J., Jackson, R., Glimcher, L, Dorf, M., Minami, M, Makino, S, Moriwaki, K, Kuzuya, H, Imura, H, et, al. (1986). The NOD mouse: recessive diabetogenic gene in the major histocompatibility complex. Science 231: 733-735 [Abstract]  
• Benacerraf, B (1981). Role of MHC gene products in immune regulation. Science 212: 1229-1238  
• BLATTNER, W. A., GARBER, J. E., MANN, D. L., McKEEN, E. A., HENSON, R., McGUIRE, D. B., FISHER, W. B., BAUMAN, A. W., GOLDIN, L. R., FRAUMENI, J. F. Jr. (1980). Waldenstrom's Macroglobulinemia and Autoimmune Disease in a Family. ANN INTERN MED 93: 830-832 [Abstract]  
• Benacerraf, B., Dorf, M. E. (1977). Genetic Control of Specific Immune Responses and Immune Suppressions by I-region Genes. Cold Spring Harb Symp Quant Biol 41: 465-475 [Abstract]  

Home | Help | Feedback | Subscriptions | Archive | Search

TABLE OF CONTENTS