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B 1h stimulates mouse spleen b lymphocytes as demonstrated by increased thymidine incorporation and formation of b cell blasts

, : B 1h stimulates mouse spleen b lymphocytes as demonstrated by increased thymidine incorporation and formation of b cell blasts. Immunobiology 160(3-4): 289-301

A few years ago, mouse spleen cells (MSPC) were found to be stimulated by human complement component C3 preparations. Using a more recently produced, .beta.1H-free C3, no significant increase of MSPC DNA synthesis was noted. C3b, which was produced by trypsin cleavage of purified C3, did not significantly stimulate 3H-thymidine incorporation and blast formation. In contrast to C3 and C3b, the .beta.1H-preparation, which showed only 1 band on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, caused very clear stimulation rates of MSPC and human tonsil lymphocytes. Since lymphocytes of C3H/He mice which did not respond to lipopolysaccharide (LPS) could be similarly stimulated by the .beta.1H-preparation, LPS apparently was not the active substance. The .beta.1H-induced DNA-synthesis was maximal after culture for 70-92 h. The optimal concentration was .apprx. 400 .mu.g .beta.1H/ml. Thymidine incorporation also could be increased in the absence of fetal calf serum (FCS), but the addition of increasing amounts of FCS clearly enhanced the .beta.1H effect. After 92 h of culturing, 15-25% of the MSPC became blasts. Of these blasts, 65-75% could be stained with fluorescein isothiocyanate(FITC)-conjugated anti-mouse IgM, while they could not be labeled with FITC-conjugated anti-mouse Thy 1.2. These results, together with the finding that removal of complement receptor-positive (CR+) cells from the spleen cell suspension dramatically reduced the DNA-synthesis, suggest that CR+ cells, like B cells and/or macrophages, are the main target cells of the .beta.1H effect. Mechanisms possibly underlying the .beta.1H effect are discussed. Binding of .beta.1H to .beta.1H receptor is one possibility.

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