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CX 3 CL 1 in allergic diseases: not just a chemotactic molecule
Author(s) -
Julia V.
Publication year - 2012
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/j.1398-9995.2012.02870.x
Subject(s) - chemokine , chemotaxis , immunology , pathogenesis , asthma , atopic dermatitis , chemokine receptor , chemistry , receptor , medicine , biology , inflammation , biochemistry
Allergic asthma and atopic dermatitis ( AD ) are two allergic diseases that are primarily driven by the activation of T helper ( T h)2 cells. T h2 cells produce cytokines that directly contribute to the symptoms of these diseases. The recruitment and maintenance of T h2 cells into the target tissues are two key events in the pathogenesis of allergic asthma and AD. While migration is mediated by both chemokines and lipid mediators such as leukotrienes and prostaglandins, very little is known about the molecules involved in lymphocyte survival and maintenance in inflamed tissues. However, chemokines could also play a role in this phenomenon. An example of this could be illustrated by CX 3 CL 1, also known as fractalkine. CX 3 CL 1 is a chemokine that is upregulated in some inflammatory diseases including allergic pathologies and that was recently demonstrated to provide a survival signal upon binding to its unique receptor CX 3 CR 1.