ABSTRACT
DBA/2J spleen and peritoneal cells were compared for their ability to present the minor lymphocyte stimulatory superantigen Mls-1a. Although capable of Mls presentation in vivo, peritoneal cells were less effective than spleen cells in vitro. This difference was not due to cell concentration or culture duration. Flow cytometric comparison of spleen and peritoneal B cells revealed no significant differences in cell surface markers needed for cognate interaction with T cells. Resolution of peritoneal B cell subsets by cell sorting revealed that even though B-1 cells were capable of Mls presentation, they were less effective than B-2 cells. Mixing experiments showed that B-1 cells did not inhibit B-2 cell presentation of Mls. In contrast, total peritoneal cells inhibited T cell responses to Mls presented by spleen cells. The peritoneal cavity harbors B cells that can present Mls as well as other cells that can suppress this response.
Subject(s)
Antigen Presentation/immunology , B-Lymphocytes/immunology , Minor Lymphocyte Stimulatory Antigens/immunology , Peritoneal Cavity/cytology , Animals , Female , Male , Mice , Mice, Inbred Strains , Minor Lymphocyte Stimulatory Antigens/metabolism , Spleen/cytology , Spleen/immunologyABSTRACT
Comparative analyses of the ability of lymphoid tissue to present the minor lymphocyte stimulatory (Mls) superantigen Mls-1a in vitro revealed that all tissues containing mature B cells, except peritoneal cavity (PerC) cells, induced Mls-1a-specific T cell activation. Irradiation and mitomycin C treatment, addition of IL-2 and IL-12, and neutralization of IL-10 and TGF-beta did not restore Mls-1a antigen presentation by PerC cells. Co-culture studies revealed that PerC cells actively suppress the T cell response to Mls-1a. PerC cells from severe-combined immune-defective (SCID) mice also suppressed this response indicating that nonlymphoid cells mediate this effect. These results suggest that in addition to antigen processing and presentation, resident peritoneal cavity cells may temper lymphocyte activation.
Subject(s)
Antigen-Presenting Cells/immunology , Immune Tolerance , Lymphocyte Activation/immunology , Minor Lymphocyte Stimulatory Antigens/immunology , Peritoneal Cavity/cytology , T-Lymphocytes/immunology , Animals , Antibodies, Monoclonal/immunology , Antigen-Presenting Cells/drug effects , Antigen-Presenting Cells/radiation effects , Apoptosis , B-Lymphocytes/immunology , Cell Communication/immunology , Coculture Techniques , Cytokines/immunology , Cytokines/pharmacology , Cytokines/physiology , Female , Lymphoid Tissue/cytology , Lymphoid Tissue/immunology , Male , Mice , Mice, Inbred Strains , Mice, Mutant Strains , Mitomycin/pharmacologyABSTRACT
The influence of age on B lymphocyte phenotype and function in DBA/2J mice was examined. The B cells of this strain express the endogenous minor lymphocyte stimulatory (Mls) retroviral superantigen (SAg) Mls-1a permitting assessment of age-related changes in cognate B cell-T cell interaction. Relative to young DBA/2J mice (< 8 months), old mice (> 17 months) had greater numbers of B cells expressing high levels of IgM and low levels of the CD11b and CD5 antigens characteristic of B-1 B cells. As measured by the T cell proliferative response to Mls, the B cells from old DBA/2J mice had reduced ability to present SAg. Upon interaction with Mls-activated T cells, old B cells secreted more IgM while young B cells made more IgG1, IgG3, and IgG2a. DBA/2J BCL functioned poorly as Mls APCs and made considerably less serum Ig. T cells from old mice exhibited a lower response to SAg and were less capable of promoting B cell differentiation. These results indicate that aging influences the cellular collaboration necessary for humoral immunity.
