DOWN-REGULATION OF MEMBRANE IMMUNOGLOBULIN-ASSOCIATED PROTEINS, MB-1,B29 AND LYN, IN AIDS-LYMPHOMAS AND RELATED CONDITIONS

B-lymphocytes infected with Epstein-Barr virus (EBV) can proliferate i n immunocompromized hosts to form lymphomas (MLs). Similar MLs are pro duced in mice with severe combined immune deficiency (SCID) by transfu sion of human lymphocytes infected with EBV (SCID-EBV-positive BML). M b-1 and B29 are recently found transmembrane proteins associated with membrane immunoglobulins (mig) on the surface of B cells. Lyn is a src family gene product expressed in B cells submembranously, in associat ion with mIg, possibly through Mb-1/B29 heterodimer. These mIg-associa ted proteins (Mb-1, B29 and Lyn) are known to mediate antigenic stimul ation through mIgs. We noted recently that Lyn is decreased selectivel y in around a half of SCID-EBV-positive BMLs. We extended this line of investigation to other mIg-associated proteins. Five acquired immunod eficiency syndrome (AIDS)-MLs and ten SCID-EBV-positive BMLs were firs t analysed by immunohistochemistry for the expression of Mb-1, B29 and Lyn. It was found that in AIDS-MLs, all the mIg-associated proteins w ere heavily down-regulated. In SCID-EBV-positive BMLs, Mb-1 was down r egulated in six of ten, B29 in nine of ten and Lyn in six of ten, wher eas no down-regulation was noted in eight EBV-free B MLs that were als o maintained in SCID mice. An additional flow-cytometric study of two SCID-EBV-positive and two EBV-negative BMLs showed similar down-regula tion in the former cases exclusively. Whereas mig was also decreased i n three of five SCID-EBV positive BMLs, it did not necessarily match t he decrease of mIg-associated proteins, which contrasts with the recen t finding that mIgs co-exist with Mb-1 or B29. Some EBV-encoded protei ns may activate host molecules located downwardly; this, in turn, may lead to the suppression of these upwardly-located mIg-associated prote ins.