Developmental coupling of expression of the ighlinked minor antigen H-40 to membrane immunoglobulin expression

C.B-20 (Igh^b) but not BALB/c (Igh^a) mice are able to reject BCL₁, a spontaneous B cell leukemia of BALB/c origin. The protective immune response is directed to1 ward the minor histocompatibility (H) antigen, H-40, which can be detected by cytotoxic T lymphocytes and is expressed on surface (s) immunoglobulin positive tumor cells including BCL₁ as well as slg⁺ lymphoblasts activated by lipopolysaccharide. The fact that only slg⁺ tumor cells and lymphoblasts express H-40 suggests that slg itself may be a component involved in CTL recognition of this antigen. However, this possibility was ruled out by demonstrating that removal of slg from target cells did not prevent H-40-specific CTL recognition. To determine whether H-40 expression was coordinately regulated with that of membrane Ig, we determined whether H-40^- slg¹ cells acquire H-40 when induced to express slg. We also transfected a functional μ c and v region gene into a slg^- lymphoma so that it acquired a slg⁺ phenotype. In neither case did such slg⁺ cells acquire H-40. Together, these data indicate that H-40 is expressed on B cells representing a particular stage of differentiation that is coincidental with slg. We previously showed that H-40 and Igh loci are linked on the 12th murine chromosome. In this study we further localized H-40 to a point beyond Aat (formerly Pre-1) near Lm-1, a locus previously described to encode minor H-antigens expressed on lymphomyeloid cells. Thus, H-40 and Lm-1 may represent a gene cluster encoding antigens expressed on subsets of lymphoid and myeloid cells.