A new serologically defined locus,Qa-1, in theTla-region of the mouse

Qa-1 restriction of CD8+ suppressor T cells

“…Early work revealed an inhibitory interaction between CD8 + and CD4 + T cells in vitro that depended on the expression of the Qa-1 molecule on activated CD4 + target cells (21). The significance of this observation became clearer after Qa-1 was shown to be a peptide-binding class Ib molecule (rather than an activation-related surface protein); it mapped to the 3′ end of the MHC class I region on chromosome 17, the same region that contained other class Ib genes, including thymus leukemia antigen (22)(23)(24). The mouse MHC class Ib molecule Qa-1 and its human homologue, the HLA-E protein, form heterodimers with β 2 m in lymphoid cells that bind to and present peptides derived from self or foreign proteins (25)(26)(27)(28).…”

T-CELL-SPECIFIC MURINE Ia ANTIGENS: SEROLOGY OF I-J and I-E SUBREGION SPECIFICITIES

“…B10.A(5R), derived from B10.A (Qa-l+), differs at this locus from B10 and B10.D2 (both Qa-1-) (37). However, test strains B10.HTT and BI0.BR (Qa-1-) cannot react by virtue of the Qa-1 antigen, indicating that the specificities detected are not products of this locus.…”

Genetic control of radiation leukemia virus-induced tumorigenesis. I. Role of the major murine histocompatibility complex, H-2.

“…In this comparison, TL" is associated with susceptibility and TL b with resistance, whereas these alleles are in all other cases associated with resistance and susceptibility, respectively. Nonetheless, it cannot be argued definitively that loci within the segment of chromosome between TL and D, such as Qa-1 (14) and Qa-2 (15) or TL proper are not involved in conferring resistance to RadLVinduced neoplasia. The available TL congenic strains C57BL/6 and C57BL/6-TL" do not differ significantly in susceptibility to RadLV-induced neoplasia (data not shown).…”