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The Substance P and Somatostatin Interferon‐γ Immunoregulatory Circuit a
Author(s) -
WEINSTOCK JOEL V.,
ELLIOTT DAVID
Publication year - 1998
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1998.tb09592.x
Subject(s) - granuloma , somatostatin , interferon gamma , macrophage , inflammation , schistosoma mansoni , cytokine , immunology , biology , interferon , schistosomiasis , pathology , medicine , endocrinology , in vitro , helminths , biochemistry
A bstract : Murine schistosomiasis mansoni is a parasitic disease in which flukes living in the portal vein of the host produce ova that deposit in the liver and intestines. In these organs, ova release antigens that induce chronic, focal granulomatous inflammation. IFN‐γ is an inflammatory cytokine important in macrophage activation and B‐cell differentiation. A substance P (SP)/somatostatin (SOM) neurokine immunoregulatory circuit controls IFN‐γ production in schistosome granulomas. SP stimulates, while SOM inhibits IFN‐γ release, modulating IFN‐γ‐dependent circuitry. SP and SOM function through interaction with authentic SP and SOM receptors located on granuloma T cells. Also, the granulomas produce authentic SP and SOM14, as evidenced by the presence of mRNA and product. The granulomas have no nerves. This and other data suggest that the inflammatory cells make these neurokines. Granuloma macrophages produce SOM. Macrophages from various sources express SOM mRNA in response to LPS, IFN‐γ, IL‐10 or several other inflammatory mediators. Thus, the inflammation of murine schistosomiasis has a complete SP/SOM immunoregulatory circuit, which in turn is subject to immunoregulation.