1. An immune paradox: How can the same chemokine axis regulate both immune tolerance and activation?
- Author
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Kevin A. Fenix, Shaun R. McColl, Julie A. Brazzatti, Michelle E Turvey, Phillip Nguyen, Ervin E. Kara, Yuka Harata-Lee, Mark D. Bunting, Iain Comerford, Sarah Haylock-Jacobs, Wendel Litchfield, and Carly E. Gregor
- Subjects
Inflammation ,Receptors, CCR6 ,CCR1 ,Chemokine CCL20 ,biology ,Chemokine receptor CCR5 ,T-Lymphocytes ,CCL18 ,hemic and immune systems ,chemical and pharmacologic phenomena ,C-C chemokine receptor type 6 ,Adaptive Immunity ,T-Lymphocytes, Regulatory ,General Biochemistry, Genetics and Molecular Biology ,Autoimmune Diseases ,CCL20 ,Chemokine receptor ,Immunology ,Immune Tolerance ,biology.protein ,Humans ,Th17 Cells ,CCL13 ,CCL21 - Abstract
Chemokines (chemotactic cytokines) drive and direct leukocyte traffic. New evidence suggests that the unusual CCR6/CCL20 chemokine receptor/ligand axis provides key homing signals for recently identified cells of the adaptive immune system, recruiting both pro-inflammatory and suppressive T cell subsets. Thus CCR6 and CCL20 have been recently implicated in various human pathologies, particularly in autoimmune disease. These studies have revealed that targeting CCR6/CCL20 can enhance or inhibit autoimmune disease depending on the cellular basis of pathogenesis and the cell subtype most affected through different CCR6/CCL20 manipulations. Here, we discuss the significance of this chemokine receptor/ligand axis in immune and inflammatory functions, consider the potential for targeting CCR6/CCL20 in human autoimmunity and propose that the shared evolutionary origins of pro-inflammatory and regulatory T cells may contribute to the reason why both immune activation and regulation might be controlled through the same chemokine pathway.
- Published
- 2010
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