NDLI: Disruption of the complement anaphylatoxin receptor C5L2 exacerbates inflammation in allergic contact dermatitis.

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Disruption of the complement anaphylatoxin receptor C5L2 exacerbates inflammation in allergic contact dermatitis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wang, Ruobing Gerard, Norma P. Lu, Bao Gerard, Craig
Description	Author Affiliation: Wang R ( Ina Sue Perlmutter Laboratory, Division of Respiratory Diseases, Department of Pediatrics, Children's Hospital, Boston, MA 02115)
Abstract	The complement anaphylatoxin C5a is a critical mediator of allergic contact dermatitis, bridging essential aspects of innate and adaptive immunity. This anaphylatoxin functions by interacting with two 7-transmembrane segment receptors, the C5aR and C5L2. The C5aR is a classical G protein coupled receptor, whereas C5L2 is deficient in coupling to G proteins because of variations in the sequence. Our previous work in human neutrophils revealed a unique role for C5L2 in negatively modulating anaphylatoxin receptor mediated cellular activation through interactions with ß-arrestin. When C5L2 is deficient, C5aR-mediated ß-arrestin signaling is greatly enhanced. The work described in this study was undertaken first to determine the effect of C5L2 deficiency in a murine model of contact sensitivity, and second to determine whether the resultant exacerbation of inflammatory parameters reflects a negative modulatory function of C5L2 on the C5aR. First, we find dramatic increases in inflammation in C5L2(-/-) animals compared with wild type mice. Second, these increases are completely reversed following administration of mAb against the C5aR. Thus, in allergic contact sensitivity, as in isolated human neutrophils, C5L2 functions to suppress C5a-C5aR-mediated responses, further underscoring its role as a negative regulator of anaphylatoxin activity.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1301626
Journal	The Journal of Immunology
Issue Number	8
Volume Number	191
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-10-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Complement C5a Immunology Dermatitis, Allergic Contact Inflammation Receptor, Anaphylatoxin C5a Receptors, Chemokine Animals Antibodies, Monoclonal Arrestins Metabolism Lymph Nodes Cytology Mice Mice, Inbred Balb C Mice, Knockout Antagonists & Inhibitors Deficiency Genetics Signal Transduction Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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