Synthesis of acute phase proteins

Most acute phase proteins are synthesized in the liver, although the genes for some are also expressed in cells and tissues elsewhere. Transcriptional control is the main mechanism for regulation of production but mRNA stability contributes in some cases. A large number of cytokines, including interleukin l (IL-1), IL-6, tumor necrosis factor a and various interferons, are capable of inducing increased, or in some cases decreased, production of various acute phase proteins in vivo and in cultured hepatocytes and liver cell lines in vitro. Glucocorticoids and steroid sex hormones can play an important permissive role and neural and neuroendocrine influences may be significant in vivo. Results obtained in different laboratories with different acute phase proteins, different cytokines and different cell lines or experimental systems have shown much variation. It has been difficult to reconcile all the findings and to identify the critical participation of particular mediators in control of particular reactants, especially because of the cascade effects by which some cytokines promote the production of others. Nevertheless it is striking that IL-6 knockout mice mount absolutely no acute phase response of serum amyloid A protein (SAA), serum amyloid P component (SAP) or complement component C3 following induction of sterile inflammation by casein or silver nitrate injection, whereas lipopolysaccharide (I.PS) induces a definite, although subnormal, response.

Studies with transgenic mice bearing the human CRP gene, with transfected cells containing human SAA genes, and with hepatoma ccll lines, have identified regulatory flanking regions of DNA which are targets for the action of nuclear factors responsive to IL-6 and IL-1.

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