Neuroendocrine-Immune Disturbances in Animal Models with Spontaneous Autoimmune Diseasesa

Authors

  • GEORG WICK,

    Corresponding author
    1. Institute for General and Experimental Pathology, University of Innsbruck, Medical School, Fritz-Pregl-Strasse 3, A-6020 Innsbruck, Austria
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  • ROSWITHA SGONC,

    1. Institute for General and Experimental Pathology, University of Innsbruck, Medical School, Fritz-Pregl-Strasse 3, A-6020 Innsbruck, Austria
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  • OSKAR LECHNER

    1. Institute for General and Experimental Pathology, University of Innsbruck, Medical School, Fritz-Pregl-Strasse 3, A-6020 Innsbruck, Austria
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  • a

    This work was supported by a grant from the Austrian Ministry of Science, Traffic and Art within the framework of the Austrian-French Program for Scientific Cooperation. Oskar Lechner is a recipient of a doctoral fellowship of the Austrian Academy of Sciences.

Additional correspondence information: Telephone: 0043-512-507-3100; Fax: 0043-512-507-2867.

Abstract

Abstract: According to our concept, the development of autoimmune diseases depends on the presence of two sets of essential genes, one coding for an abnormal autoreactivity of the immune system, the other for a primary susceptibility of the target organ/structure for the immune attack. The final outcome of the disease in a given individual is then fine tuned by modulatory factors, such as diet or hormones. With regard to the latter, the immuno-endocrine interaction via the hypothalamo-pituitary-adrenal (HPA) axis has proven to be of special importance. Investigating the so-called Obese strain (OS) of chickens, an animal model with a spontaneously occurring Hashimoto-like autoimmune thyroiditis, we have first shown an impaired surge of glucocorticoid hormones after stimulation of the HPA axis by antigens or certain cytokines (glucocorticoid-increasing factors-GIFs). More recently, we have found a similar behavior in models with systemic autoimmune diseases, that is, murine lupus erythematosus and avian scleroderma. More detailed studies have, however, proven that the mechanisms underlying this altered immuno-endocrine communication via the HPA axis differs in different models. Finally, recent data point to the possibility that the classical pathways of glucocorticoid-T-cell interactions also take place in the thymus itself, which has been shown to be a site of steroid hormone production.

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