SPECIFIC INHIBITION OF LYMPHOID COMPLEMENT RECEPTORS BY ANTI‐H‐2 SERA: EVIDENCE FOR A NEW H‐2 LINKED POLYMORPHISM

Certain anti‐H‐2 sera contain an antibody‐like activity which specifically inhibits EAC rosette formation by lymphoid (and not myeloid) cells of certain mouse strains. Studies in congenic recombinant mouse strains strongly indicate that at least part of the control of susceptibility to inhibition by these antisera is mediated by H‐2 linked genes, mapping in the I‐C subregion or the S region. The strain distribution of the trait CRIS indicates that certain H‐2 identical mice behave differently from one another, pointing toward a component of non‐H‐2 modulation of the H‐2 linked gene (or to a previously unsuspected H‐2 difference). Positive sera were usually raised across differences in the D end of the H‐2 complex. The complex implications of this system must be considered in the light of known S region involvement in complement metabolism.