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Related post: other animals and in man. On recognition of the regulatory role which the MHC exerts on the immune system, efforts to clarify the responsible mechanisms have intensified. To facilitate research in this area, the program has contractually supported the 5-11 acquistion and distribution of antisera with specificities against various mouse cell surface antigens. A supply of antiserum against many of the H-2 gene products has been made available for distribution to investigators through a contract Buy Fulvicin awarded to Chella S. David (AI 8-2564, Mayo Foundation). Similarly, antisera specific for antigens of the I region of the H-2 complex have been prepared by Donald C. Shreffler (AI 6-2502, Washington University) and are available for distribution to investigators. Evidence obtained in several experimental systems has convincingly demonstrated that efficient physiological interactions among macrophages, T cells, and B cells require that these cells share membrane molecules encoded for by the MHC of the species. Dr. David H. Katz (AI 13874, Scripps Clinic and Research Foundation) has provided substantial evidence that the genes controlling interactions between T and B lymphocytes are located in the I region of the mouse H-2 complex. He has found that T lymphocytes will not exert effective helper functions for B cells when these cells differ at the relevant I region locus. He believes that self- recognition is the critical mechanism by which cell-cell communication takes place in the immune system. In a related project (AI 13781), he has obtained evidence indicating that the process of differentiation of stem cells and their progeny also may be critically regulated by MHC gene products. Using bone marrow chimeras, he has demonstrated that lymphocyte differentiation may be "adaptive" to the environment in which it takes place. He believes such an "adaptive differen- tation" results in preferential interactions among cells that have undergone their differentiative processes in the same genotypic environment; "adaptive differentiation" thus may represent a manipulative approach to define genetic and molecular mechanisms responsible for cell-cell interactions. Genetic restrictions imposed by products of the I region of the H-2 complex on interactions between macrophages and immune T cells are being investigated by Carl W. Pierce (AI 13915, Jewish Hospital of St. Louis). Using antigen pulsed macrophages, he has found that naive lymphocytes will respond to antigen even if it is presented on a histoincompatible macrophage. However, the secondary immune response is genetically restricted; the immune T cell must be stimulated with antigen-bearing macrophages which are genetically identical to the macrophage that presented the antigen during the primary immunization. He has demonstrated that such genetic restrictions are controlled by products of the I-A subregion of the H-2 complex and believes that these restrictions involve active suppressive phenomena when antigen is presented on an inappropriate macrophage. In a related study, Judith A. Kapp-Pierce (AI 13987, Jewish Hospital of St. Louis) has found that an antigen specific suppressor T cell factor is activated when nonresponder lymphocytes are stimulated by antigen; suppres- sion by this factor is mediated by a molecule encoded by the I-J subregion of the H-2 complex. She also has shown that this suppressor factor does not require participation of macrophages for effective suppression; she suggests that the suppressor factor acts directly on primed B cells. The results of similar studies by Donal B. Murphy (AI 14349, Yale University) suggest that the different functional subpopulations of immunocompetent lymphocytes express different products of the I region on their surface. He has demonstrated that suppressor T cells bear an I region antigen not found on helper T lymphocytes. 5-12 Of interest is his observation that, although different T cell subpopulations bear distinct I region products, all or many of these products appear to be expressed on the surface of the macrophage so that its interaction with these lymphocytes would not be encumbered by this type of genetic restriction. Cell -cell interactions are required not only to initiate the immune response but also to regulate it. It is now recognized that the help and suppression provided by T cell subsets is carefully balanced within the responding host. As demonstrated by Richard K. Gershon (AI 10497, Yale University), helper T cells, on stimulating B cells to produce antibody, also become susceptible to regulation through a feedback inhibition mechanism by inducing suppressor T cells. In collaboration with Harvey Cantor (AI 13600, Sidney Farber Cancer Institute), the functional subsets have been identified on the basis of the Ly differentiation antigens present on their surfaces. Thus, helper cells have been shown to be Ly 1+ while suppressor cells are Ly 2, 3+. Dr. Cantor recently has provided convincing evidence that the Ly 1 helper cell can induce an uncommitted Ly 1, 2, 3+ subset to participate in specific suppressor activity. In this context. Dr. Gershon believes from his current studies on the cellular feedback inhibition mecha- nism that suppressor dysfunction is a cause of at least some autoimmune diseases. Dr. Cantor has demonstrated recently that feedback inhibition is induced by Ly 1+ cells which also express the Qa 1 cell surface molecule and that selective stimulation of Ly 1+ cells which lack the Qa 1 antigen can negate feedback inhibition mechanisms. Functionally distinct T cell subsets have also been identified in humans using monoclonal antibodies prepared against human thymocytes. Evidence is accumulating that the T4 antigen is present on a mature T cell subset in the peripheral blood population which has helper function; reciprocally, the pre- sence of the T5 cell surface antigen has been correlated with the suppressor population of peripheral T cells. Dr. Cornelius P. Terhorst (AI 15066, Sidney Farber Cancer Institute) has provided physicochemical evidence that the T4 and T5 antigens are the human homologs, respectively, of the murine Ly 1 and Ly 2, 3 antigens. He has found that the T4 and T5 antigens can be isolated using antisera against murine Ly antigens and that the isolated human antigens have molecular size and structural features comparable to those of murine T cells. Although research on functional subsets of T lymphocytes is proceeding at an accelerated pace, it is recognized that this work is technically limited by the need to separate the subsets in adequate numbers for study. This difficulty may be obviated by the recent work of Frank W. Fitch (AI 04197,
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