Effects of Experimental Allergic Encephalomyelitis on Thymus and Adrenal: Relation to Remission and Relapse

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Abstract
Experimental allergic encephalomyelitis (EAE) was induced by active immunization with neural tissue and adjuvants and by passive transfer of living lymphoid cells. Severe thymolysis occurred along with severe clinical signs and lesions. Thymolysis was preceded and accompanied by a striking rise in serum corticosterone. Clinical signs then remitted, followed by a decline in serum corticosterone and beginning regeneration of the thymus, but histologic EAE lesions persisted. Adrenalectomy performed early in the remission of EAE was followed promptly by disappearance of serum corticosterone and relapses of clinical signs. Relapses occurred in rats of either sex but not until thymic regeneration had begun. All these data support the theory that nonspecific stress and the state of adrenal hyperactivity in response to neurological disability determine patterns of remission and relapse in EAE by way of immunosuppressive effects on lymphoid tissue.

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