Human C5a and C5a analogs as probes of the neutrophil C5a receptor☆
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Complement and thrombosis in the antiphospholipid syndrome
2016, Autoimmunity ReviewsCitation Excerpt :Briefly, complement-derived inflammatory mediators (anaphylatoxins) such as C4a, C3a, and C5a mainly contribute to the pathophysiology of complement-induced placentae inflammation. They increase vascular permeability, activate platelets or neutrophils [4], and promote the release of cytokines such as tumour necrosis factor (TNF) alpha from monocytes [5], which secondarily induces and accelerates systemic inflammation and coagulation. The involvement of the complement system in the manifestation of pregnancy morbidities in patients with APS was suggested from the analysis of the histopahology in the placentae of women with aPL [6] or by the registry of the patients [7].
C5a and pain development: An old molecule, a new target
2016, Pharmacological ResearchCitation Excerpt :These C5a activities are exerted by interacting with high affinity (Kd of approximately 1 nM) with its selective receptor C5aR, also called CD88, which is a class A seven-transmembrane G-protein-coupled receptor (7TM GPCR) [38–41]. C5aR was initially identified in neutrophils, eosinophils, monocytes, dendritic cells and mast cells [42–44]. It is now known that it is also expressed in non-immune cells, such as the vascular endothelium [27], astrocytes [45], microglia [46], oligodendrocytes [47], primary sensory neurons of the dorsal root ganglion [48], neural stem cells [49], synovial cells [50], articular chondrocytes [51] and others.
Purification and functional assessment of C3a, C4a and C5a of the common carp (Cyprinus carpio) complement
2004, Developmental and Comparative ImmunologyRole of the second extracellular loop of human C3a receptor in agonist binding and receptor function
1999, Journal of Biological ChemistryResidues 21-30 within the extracellular N-terminal region of the C5a receptor represent a binding domain for the C5a anaphylatoxin
1998, Journal of Biological Chemistry
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This is publication number 1800 from the Research Institute of Scripps Clinic. This work was supported by USPHS grant HL 20220, program project grants HL 16411,1 S07 RR-05514 and a grant from the Council for Tobacco Research (No. CTR 1105). Dr. Chenoweth was supported in part by USPHS grant GM 02179.