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Notes: Summary The thymus produces a nonapeptide capable of inducing T cell surface markers and T cell functions in immature lymphoid cells. This peptide is found partly bound to a carrier protein in the circulation from where it has been isolated (hence its name of serum thymic factor (FTS)). Immunofluorescence studies using an antibody raised against synthetic FTS has shown that it is produced by the thymic epithelium. Its mode of action at the cellular level involves the binding to specific high affinity receptors.

Notes: Abstract Most immunologically-mediated diseases are inflammatory in nature, as assessed by cellular infiltrates at the lesion site. Recent immunohistological studies using monoclonal antibodies on tissue sections and synovial or cerebrospinal fluid reveal that B- and T-lymphocytes (predominantly T) participate in this reaction, together with monocytes and macrophages. The etiopathogenesis of inflammatory diseases of immunological origin can be discussed at two levels. (1)Lesions may be secondary to the cytopathic effect of antibodies, either by direct cytolysis or by opsonization, antigenic modulation, or blockage of functionally-relevant molecules. Immune complexes formed in the circulation or locally at the lesion site may intervene. Direct cellular mechanisms are probably involved, as suggested by evidence in hepatitis (indirect) and in juvenile insulin-dependent diabetes (direct). K-cells may act by antibody-dependent cytotoxic'ty, paritularly in autoimmune diabetes and thyroiditis where lymphocyte-dependent antibodies are demonstrated. Unfortunately, the absence of adequate markers does not permit adequate detection of K-cells in inflammatory reaction sites. (2)Etiological factors are multiple in a given disease and even in a single patient. Deficiency of suppressor T-cells, assessed using monoclonal anti T-cell antibodies, represents a major predisposing factor, although suppressor cell deficit may be restricted to some antigens (EBV) in certain patients. The deficiency of interleukin-2 production in lupus and rheumatoid arthritis is intriguing but the mechanism and its relationship to disease etiology are unknown. Other immunological factors include intrinsic B-cell hyperactivity, anti-T-cell auto-antibodies, and complement deficiencies, whereas non-immunological factors such as viruses, drugs or sex hormones are important but ill-defined. The treatment of immunologically-mediated inflammatory diseases can be considered at several levels. Anti-inflammatory agents act peripherally, and where only anti-inflammatory action is needed, NSAIDs should be used. Immunosuppressive agents act non-specifically and a better appreciation of their respective immunosuppressive and anti-inflammatory actions is required, especially for steroids. More selective drugs are needed, such as cyclosporin A which acts selectively on helper T-ce!ls or monoclonal anti-T-cell antibodies. Immunomodulating drugs such as the thymic hormones, which would allow restoration of the physiological T-cell balance, represent a new approach and preliminary data in murine lupus and human rheumatoid arthritis are promising.