Peripheral corticotropin-releasing hormone and urocortin in the control of the immune response.
Immunological and cellular stress signals trigger the release of corticotropin-releasing hormone (CRH) from the spleen, thymus and inflamed tissue. In vivo and in vitro studies generally suggest that peripheral, immune CRH has pro-inflammatory effects and acts in a paracrine manner by binding to CRH-R1 and CRH-R2 receptors on neighboring immune cells. However, it now seems likely that some of the suggested pro-inflammatory actions of CRH may be attributed to novel CRH-like peptides or to the related peptide, urocortin, which is also present in immune cells and has especially high affinity for CRH-R2 receptors.
Baigent
S M
SM
School of Animal and Microbial Sciences, University of Reading, Whiteknights, RG6 6AJ, Reading, United Kingdom. s.m.baigent@reading.ac.uk
D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology; D003346:Corticotropin-Releasing Hormone / Q000737:chemistry / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D007111:Immunity, Cellular / Q000502:physiology; D007249:Inflammation / Q000276:immunology*; D018019:Receptors, Corticotropin-Releasing Hormone / Q000737:chemistry* / Q000502:physiology; D013154:Spleen / Q000276:immunology; D013950:Thymus Gland / Q000276:immunology; D015854:Up-Regulation; D054832:Urocortins
D018019:Receptors, Corticotropin-Releasing Hormone; D054832:Urocortins; D003346:Corticotropin-Releasing Hormone