Different macrophage requirement in the specific and polyclonal responses induced by TNP-LPS and LPS.
The in vitro anti-trinitrophenyl (TNP) response induced by TNP-lipopolysaccharide (TNP-LPs) in mouse spleen cells was eliminated by passage through Sephadex G10 columns. Conditioned medium obtained from peritoneal macrophages restored the response, indicating the supportive role of such cells in the response. Conversely, polyclonal B-cell activation mediated by LPS was not affected by Sephadex G10 treatment, as judged by incorporation of 3H-thymidine, generation of specific anti-TNP plaque-forming cells, and induction of polyclonal IgM-secreting cells. The failure of the LPS  moiety of TNP-LPS to induce B-cell activation without macrophage help suggests a restriction in the number of available anti-LPS receptor molecules when the Ig anti-TNP receptor interacts with the haptenic (TNP) groups. This restriction can be due to the attachment of the TNP molecules to residues located in the vicinity of the lipid A mitogenic region of the carrier.
D000818:Animals; D000921:Antibody-Producing Cells / Q000276:immunology; D007075:Immunoglobulin M / Q000096:biosynthesis; D008070:Lipopolysaccharides / Q000276:immunology*; D008264:Macrophages / Q000276:immunology*; D008623:Mercaptoethanol / Q000494:pharmacology; D051379:Mice; D008810:Mice, Inbred C57BL; D009578:Nitrobenzenes / Q000276:immunology*; D013154:Spleen / Q000276:immunology; D014301:Trinitrobenzenes / Q000276:immunology*
D007075:Immunoglobulin M; D008070:Lipopolysaccharides; D009578:Nitrobenzenes; D014301:Trinitrobenzenes; D008623:Mercaptoethanol