Con A-induced IL-2 Production Research Articles

Mechanism of action of the new immunomodulator LS2616 on T cell responses

Spleen cells from mice treated with LS2616 display a highly increased response to the polyclonal T cell lectin ConA. The total number of splenic T cells, and the relative ratios between L3T4 + and Lyt-2 + T cells were not altered by LS2616 treatment. By dissecting the overall ConA response it was found that the number of ConA-inducible, IL-2 reactive T cells was unaffected, while ConA-induced IL-2 production was enhanced after LS2616 treatment. Spleen cells from LS2616 treated mice, depleted of G10 adherent macrophages (Mφ) and reconstituted with Mφ from untreated mice displayed normal levels of ConA responses. Mφ depleted spleen cells from untreated animals, cocultured with Mφ enriched populations from LS2616 treated animals resulted in an increased ConA response. Furthermore, spleen cells from treated mice were found to be excellent stimulators for alloantigen-induced T cell responses; when used as responders in MLC, however, these cells were comparable to responders from non-treated animals. Taken together the results demonstrate that LS2616 exerts an immunostimulatory effect on Mφ, which indirectly facilitates polyclonal and antigen-specific T cell responses. The possible implications of this observation on various immunoregulatory events are discussed.

T lymphocyte population dynamics and function following a primary bovine herpesvirus type-1 infection.

Following a primary bovine herpesvirus-1 (BHV-1) infection the concanavalin A (Con A) induced proliferative responses of peripheral blood T lymphocytes were suppressed. This suppression occurred in the absence of detectible serum suppressor factors, suppressor cell activity or decreased accessory cell function. However, regression analysis demonstrated a significant correlation between the percentage of T lymphocytes present within the peripheral blood mononuclear cell (PBMC) population and the amplitude of Con-A-induced lymphocyte proliferative responses (LPR). Direct evidence that a numerical deficit of responder T lymphocytes was limiting LPR was obtained by using an immunomagnetic microsphere (IMM) negative enrichment protocol to produce a PBMC population with a constant percentage (75 +/- 6%) of T lymphocytes. The Con-A-induced LPR of these enriched T lymphocytes remained constant following BHV-1 infection. Flow cytometric (FC) analysis of PBMC indicated that the decreased percentage of circulating T lymphocytes, associated with BHV-1 infection, was caused primarily by a selective depletion of the BoT8 subset. These FC data were consistent with the indirect evidence of increased TH activity, as indicated by elevated Con A-induced IL-2 production. Thus, 2 to 5 days following viral infection, the circulating T lymphocytes were activated as shown by elevated IL-2 production, increased recombinant bovine IL-2 (rBo

Activation of phagocytosis associated oxidative metabolism in human monocyte-derived macrophages exposed to bacterial products

In the present study we tested the effect of immunization with schistosome derived antigens such as frozen-thawed schistosomula in combination with either BCG, liposomes or liposomal muramyl tripeptide-phosphatidyl ethanolamine (MTP-PE), on the resistance of mice to infection, and on the function of their macrophages and lymphocytes. Immunization with either F-T schistosomula + BCG or F-T schistosomula + MTP-PE and subsequent infection, resulted in a 2–3-fold increase in adherent peritoneal macrophage-mediated schistosomulicidal activity (SCA). Peritoneal and spleen macrophages from immunostimulant treated and/or immunized animals showed a significant increase in LPS triggered TNF-α production, as compared to non-treated controls. The highest increase in TNF-α production was achieved after immunization with either F-T schistosomula + BCG or F-T schistosomula + MTP-PE. LPS triggered IL-1 production was elevated in spleen and peritoneal macrophages from F-T schistosomula + BCG treated mice, and also in spleen macrophages treated with F-T schistosomula + MTP-PE. Only immunization with F-T schistosomula + BCG increased ConA-induced spleen lymphocyte proliferation and IL-2 production. Immunization of mice with F-T schistosomula + BCG also induced protection against parasite infection, while F-T schistosomula + MTP-PE failed to do so. Potentiation of antischistosomal resistance seems to require both macrophage and lymphocyte activation which was achieved only when BCG served as an immunostimulant.