Antisera against the products of the major histocompatibility system (MHS), produced by immunization between congenic mouse strains differing only at that segment of the 17th chromosome which bears the H‐2 gene complex, exert a reproducible blocking effect on formation of rosettes with EACm (C3d rosettes). In many instances this effect is probably due to specific antibodies reactive with the lymphocytes, as indicated by immunochemical and adsorption experiments. Purified antibodies from the C3H anti‐C3H.B10 immune ascites failed to exert this blocking effect. The blocking capacity can be restored, however, by addition of fresh normal mouse, rabbit or fetal calf serum, but not by heat inactivated serum.
These experiments show that the presently defined H‐2K, H‐2D and H‐2L antigens as well as some la antigens are themselves not the C3d receptors. The blocking effects observed in the presence of complement are possibly due to the proximity of H‐2 or la molecules and C3d receptors, or to a rearrangement of membrane components after reaction with anti‐MHC antibodies and complement.