HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Forman, J. Articles by Klein, J. Search for Related Content PubMed Articles by Forman, J. Articles by Klein, J.

Immunogenetic Analysis of H-2 Mutations

II. Cellular Immunity to the H-2^Da Mutation¹

From the Department of Microbiology, The University of Texas Southwestern Medical School, Dallas, Texas 75235

Abstract

The H-2^da haplotype was derived from the H-2^d haplotype by a mutation localized to the D end of the H-2 complex. Coculture of H-2^d and H-2^da spleen cells gives rise to bidirectional MLR. However, the H-2^d anti-H-2^da response is much stronger than that of H-2^da anti-H-2^d. Both haplotypes gives rise to reciprocal CML. B10.D2(R103) strain spleen cells, which differ only at the D end of the H-2 complex from the H-2^d haplotype, kill H-2^da target cells in CML when sensitized to H-2^d stimulators and vice versa. Therefore, both the mutant and strain of origin share a D end CML specificity. H-2^d and H-2^da reject skin grafts in both directions, although some H-2^d grafts show prolonged acceptance on H-2^da recipients. These data are consistent with a mutation in the D end of the H-2^d haplotype resulting in gain-loss of an antigen(s) that gives rise to reciprocal MLR, CML, and skin graft rejection. Further, the mutant can be distinguished from the strain of origin on the basis of the strength of immune response in MLR.

Footnotes

¹ This research was supported by Grants AI11851, AI11650, and AI11879 from the National Institutes of Health.