Diagnostic implications

Data acquired in multiple studies of the in vivo levels of various SRs in health and disease, as well as following injection of cytokines, indicate that, as in cultured cells, formation of the SRs in the body is inducible by various stimulating agents. These data, particularly the evidence indicating that formation of several SRs is most strongly induced by the ligands to which they bind, are consistent with the notion that formation of the SRs constitutes a physiological mode of regulation of response. This evidence prompted investigators to employ the determination of the levels of various SRs in body fluids as a diagnostic tool for assessing disease activity and for examining the involvement of the ligand of the SR in the particular pathological situation. Information gained in this way can be particularly useful in the case of SRs that have pronounced effects on the function of their ligands. Probably the most informative diagnostic parameter in such cases is the quantitative ratio of the SRs and their ligands. Indeed, there are a few reports demonstrating correlation between the severity of a particular pathological situation to which a given cytokine contributes and the occurrence of an abnormally low quantitative ratio of SR and ligand levels in the serum.

Various cancer cells are known to shed some of their cell surface proteins far more rapidly than do their normal counterparts. This may be due to an increased expression by tumor cells of some proteases capable of cleaving these cell surface receptors. Because of this particular feature of tumor cells, and perhaps also because of the activation of certain immune cells in cancer patients, their sera exhibit increased levels of certain SRs (e.g. the soluble TNF receptors, or the carcinoembryonic antigen, which is a shed form of a GPI-anchored cell surface protein). Determination of the levels of these receptors can thus be of diagnostic value not only in inflammatory and infectious diseases but also in cancer.

See also: Antibodies, synthesis; Cytokine inhibitors; Cytokines; Cytokine receptors; Fas (CD95) and fas ligand; Fc receptors; immunoglobulin, cell surface; Immunoglobulin structure; Interferon 7 receptor; Interleukin 2 receptor; Interleukin 4 receptor; Interleu-kin 5 and its receptor; Interleukin 6 receptor; TNF receptors.

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