IMMUNOGLOBULIN AND OTHER SURFACE ANTIGENS OF CELLS OF THE IMMUNE SYSTEM

Immunoglobulins (Ig) on cells of the immune system: The cytotoxicity test, with class-specific and type-specific anti-Ig sera, identifies κ and µ determinants on mouse lymphocytes. The proportion of κ(+) cells is characteristic for each source of cells: 30% of bone marrow cells, 40% of cells from peripheral lymph nodes, 45% of lymphocytes from peripheral blood or peritoneal cavity, and 50% of spleen cells. No Ig was demonstrable on thymocytes or on leukemia cells (most of which arise from thymus-derived [T] cells). Cytotoxicity tests were performed on various myelomas secreting different Ig; the only positive reactions were given by κγ1 myelomas (all four κγ1 myelomas tested were sensitive to both anti-κ and anti-γ1). Hemolytic plaque-forming cells (PFC) of IgG type had no demonstrable surface Ig, but a proportion of IgM PFC were κ(+)µ(+). Virtually all rosette-forming cells (RFC) have surface Ig, more than 90% of them being inhibited by anti-κ, 50% by anti-µ, and 10–30% by antisera to other heavy chains. Anti-λ sera gave no positive reactions with any cell type, which is in keeping with the low level of this light chain in mouse serum. Ig and other differentiation antigens as markers for T and B cells: Thymocytes are hallmarked by the alloantigens TL, θ, and the Ly series, and it is generally held that extrathymic lymphoid cells that bear them are derived from thymocytes. There is one alloantigen marker for the thymus-independent (B) cell, and that is PC, which appears late in differentiation. (The mouse-specific lymphocyte (MSLA) and mouse-specific bone marrow-derived lymphocyte (MBLA) antigens recognized by heteroantisera, not used in the present study, are other candidates for T and B cell markers.) Making use of antisera to these surface antigens to inhibit the function of cells that carry them, we find the following: Approximately 30% of RFC, 60% of IgM PFC, and 90% of IgG are PC(+) and so are identified as B cells. No T markers were demonstrable on these cell populations. Thus if T cells do become RFC or PFC they presumably lose their T surface markers in the process (cf. the quantitative reduction of T markers accompanying the thymocyte → lymphocyte transition). Cells that have the potential to initiate graft-versus-host (GVH) reactions have the T cell surface phenotype θ(+)Ig(-). Adoptive transfer of thymus-dependent antibody-forming capacity (response to sheep erythrocytes) required θ(+) cells but transfer of a thymus-independent immune response to Brucella antigen did not. Cells with surface Ig were involved in both types of adoptive transfers. Thus the presently available T markers do not provide evidence for T cells carrying surface Ig. Suppression of the Ig phenotype by antibody: antigenic modulation? A phenotypic change from Ig(+) to Ig(-) occurs when Ig(+) lymphocytes or myeloma cells are incubated with anti-Ig sera in vitro in the absence of complement (C). As with antigenic modulation in the TL system, which it resembles, this phenomenon is temperature dependent and in the case of lymph node cells (LNC) can be inhibited by high doses of actinomycin D.