The role of the neuroendocrine system in determining genetic susceptibility to experimental allergic encephalomyelitis in the rat.

摘要: Experimental allergic encephalomyelitis (EAE) can be induced in some strains of rat but not others, by the injection guinea-pig myelin basic protein Freund's complete adjuvant. In susceptible Lewis strain, spontaneous recovery from paralysis occurs and previous studies have shown that this is dependent on production, during course disease, high levels corticosterone adrenal glands. Adrenalectomy completely abrogates phase disease becomes uniformly fatal unless steroid replacement therapy given, which reproduces serum hormone develop intact animals with EAE. The PVG strain to EAE, here it rats had been adrenalectomized developed severe they do recover. As rat, could prevent outcome case resembled seen animals. By a number parameters appear make more vigorous response stress than Lewis. A comparison ratio weight body between these indicated larger PVG, levels, stress, were also found higher strain. Furthermore, basal much labile mean value those age- sex-matched compared. Genetic analysis using congenic showed was linked major histocompatibility complex (MHC). It appears resistance EAE depends an enhanced mediates its immunosuppressive effect via While plays essential part sufficiently potent virtually signs disease. Resistance induction abrogated adrenalectomy all studied. particular, PVG.RT1u rats, same background genes as RT1u rather RT1cMHC did when glands removed.(ABSTRACT TRUNCATED AT 400 WORDS)