Aberrancy in immunogenicity and cell-surface expression of H-2 antigens on erythrocytes

Abstract

Immunogenicity for T cell-independent B-cell response assessed by splenic plaque-forming cell (PFC) response and cell-surface expression measured by laser flow cytometry of various class I H-2 antigens on mouse red blood cells (RBC) were compared. It was found that the order of magnitude of both immunogenicity and cell-surface expression on RBC is H-2Dd much greater than H-2Db greater than H-2Kd, H-2Kb. Furthermore, H-2d public antigens and H-2Ld antigens were neither immunogenic nor easily demonstrable on RBC. These findings contrasted with poor immunogenicity for PFC response (Nakashima et al. 1982, 1983) and proportionally strong expression of H-2 antigens on lymphoid cells. Immunogenicity and cell-surface expression of H-2Dd antigen on RBC were not shown to be controlled by the action of genes outside H-2D. It was therefore suggested that a number of H-2 antigens, including H-2Kd private, H-2Kb private, and H-2d public specificities are at least functionally defective on RBC. This is possibly due to the structural characteristics of the antigens. Since immunogenicity and cell-surface expression were in parallel, the expression of H-2 antigens on RBC must be dictated by a subset of B cells whose activity was assessed by PFC response. This finding supports the view that the H-2 molecules display a new category of activity which is different from their ability to activate T cells and depends on their expression on RBC.

Induction of high-grade anti-tumor immunity by use of a recombinant H-2Kb/avian erythroblastosis virus erbB gene transfectant

“…The specificity of this antibody has been extensively studied and reported [7]. The anti-H-2 b polyclonal allo-antiserum was prepared as described by immunizing C3H/HeN (H-2 k) mice with EL4 (H-2 b) thymoma [16]. Monoclonal H-2K bmonospecific antibody was purchased from the Meiji Institute of Health Science, Tokyo.…”