Abstract
Study of the mechanism of mutagenic effect of C-reactive protein, the major reactant of acute phase inflammation, showed that this protein is mitogenic for normal lymphocytes and inhibits proliferation of interleukin-2-dependent CTLL-2 cells in the presence of interleukin-2; antibodies to α-chain of interleukin-2 receptor abolish the inhibitory effect of C-reactive protein. High-affinity receptor of interleukin-2 may be assembled by interleukin-2 or C-reactive protein, but not by both ligands. Therefore, immunoregulatory effects of C-reactive protein are different during the acute phase of inflammation and remote periods of immune response. At the early stages, when the production of interleukin-2 is negligible, C-reactive protein can act as a mitogen inducing polyclonal activation of lymphocytes, while later it acts as a factor limiting clonal expansion of committed immunocompetent cells.
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