Gain/loss of poly(Glu50Tyr50)/poly(Glu60Ala30Tyr10) responsiveness in the bm12 mutant strain.

Abstract

The development of inbred strains of mutant mice is useful in ascribing specific gene functions to particular genetic loci within the regions and subregions of the H-2 complex. The B6.C-H-2bm12 (bm12) strain is of particular interest in that, compared to parental C57Bl/6Kh (B6) mice, it bears a presumptive single gene mutation altering the .**GRAPHIC**. chain encoded by the I-A subregion. bm12 Mice have gained the ability to respond to poly(Glu50Tyr50) (GT) and have lost the ability to make plaque-forming cell or delayed-type hypersensitivity responses to the closely related copolymer, poly(Glu60Ala30Tyr10) (GAT), although retaining the ability to mount a GAT-specific T cell proliferative response. This is in sharp contrast to the parental B6 strain, which is a GT nonresponder and a GAT responder. The establishment of responder status as a consequence of mutation is reported. Possible mechanisms accounting for the gain/loss of GT/GAT responsiveness in the context of a 2-step helper T cell model are discussed.