Abstract
We have investigated the cellular basis of the failure of primitive extant vertebrates, e.g. Notophthalmus viridescens, the American common newt, to respond to soluble thymus-dependent (TD) antigens, e.g. keyhole limpet hemacyanin (KLH). We have found that KLH can be used to prime for amplification of a response to a hapten, 2,4,6-trinitrophenyl (TNP) when it is conjugated to KLH, only if both the unconjugated and conjugated KLH are adsorbed onto bentonite particles. The response is monitored in terms of antigen binding cells in the spleen. Moreover, prior injection of colloidal carbon, which is actively engulfed by phagocytes throughout the body, will prevent the response from taking place. Injection of colloidal carbon diminished responses to heterologous erythrocytes and to soluble or bentonite-coated 2,4-dinitrophenylated (DNP) dextran. Comparable colloidal carbon treatment did not reduce response levels to either soluble or bentonite adsorbed TNP-lipopolysaccharide (LPS) of E. coli. We suggest that the limitation in response capacity to soluble TD antigens may be associated with regulatory phagocytes. Moreover, the phagocytic cells of this primitive vertebrate appear to mediate responses to naturally particulate TD antigens and certain thymus-independent (TI) carriers, e.g. dextran, but not to LPS.
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