Abstract
Arginine vasopressin (AVP) has been recently recognized as an immunoregulatory hormone. Here we summarize the most representative experiments and discuss results concordant with this statement. Immune cells express V1a, V1b, and V2 AVP receptors. In rats, neurointermediate pituitary lobectomy (NIL) results in permanent deficiency of neurohypophysial hormones, AVP, and oxytocin (OXT); decreases humoral and cell-mediated immune responses; reduces immune resistance to intestinal Salmonella typhimurium infection, diminishes response to T-independent and T-dependent antigens, as well as weakens severity of experimental autoimmune encephalomyelitis (EAE) and joint inflammation in adjuvant-induced arthritis (AIA). The improvement of clinical symptoms of EAE and AIA is accompanied by decreased splenic interleukin (IL) mRNA expression in NIL animals. Anterior pituitary lobectomy (AL) in rats reduces secretion of all adenohypophysial hormones but AVP serum levels remain within the normal range. These animals respond to AIA immunization with increased severity in both joint inflammation and spleen ILs mRNA overexpression. Desmopressin ((DP) a synthetic AVP V2 receptor agonist) administration to NIL-EAE animals increases the severity of clinical symptoms. The use of V1a AVP receptor antagonists decreases significantly the severity of EAE. Histological study reveals that the intestinal mucosa and gut-associated lymphoid tissue (GALT) are significantly affected by AVP deficiency. In NIL rats, villus heights, goblet cells, IgA and IgM cells, and IgA secretion were reduced, and in lamina propria, the numbers of CD4 and intraepithelial CD8 lymphocytes were decreased. Altogether, one can conclude that AVP is an important immunomodulatory hormone. Understanding related to an immune–neurohypophysial interactions requires more studies. The use of AVP receptor antagonists to control the immune responses may be helpful in the treatment of autoimmune diseases.
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