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Chemokines and Asthma

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Chemokines and Asthma
Purpose of Review: The importance of chemokines and their receptors to development and maintenance of allergic asthma is reflected in the burgeoning amount of literature currently devoted to this topic. Based on a series of selected references published during the last year, this review now summarizes recent advances and discusses the likely implications of these findings.
Recent Findings: Of particular interest are reports describing novel interactions between chemokines and both eosinophils and mast cells, including a role for CXCL5 (epithelial cell-derived neutrophil-activating peptide-78) and intracellular CCR3. New insights into TH2-cell dominance are presented in reports dealing with a range of chemokines, including CCL3 (MIP-1a), CCL4 (MIP-1β), CCL5 (RANTES), CXCL9 (Mig), and CXCL10 (IP-10). The increasing importance of structural cell participation is emphasized by reports focusing on the eotaxin family (CCL11, CCL24, and CCL26), as well as CCL17 (TARC), CCL22 (MDC), CXCL9 (Mig), and CX3CL1 (Fractalkine). A developing role for nonreceptor regulatory mechanisms is also emphasized by seminal work relating to metalloproteinases, as well as reports focusing on proteoglycans and β-Arrestin-2. Finally, significant progress in the field of asthma heritability is featured in reports relating to both known and novel genes, including those encoding CCR5 and DPP-10.
Summary: The critical influence of chemokine biology on the outcome of allergic asthma continues to be highlighted in recent reports describing novel mechanisms by which eosinophils are recruited into the lung and local TH2-cell dominance is maintained. Also of considerable interest is the increasing emphasis currently being realized for structural cell participation, nonreceptor regulatory mechanisms, and the influence of susceptibility genes.

Although notably heterogeneous in form, asthma can nonetheless be broadly defined as a clinical syndrome involving altered lung function and airway hyperresponsiveness. A major pathologic feature of asthma is chronic local inflammation resulting from selective recruitment of TH2-cells and eosinophils in a manner that correlates with disease severity. The pivotal role established for chemotactic cytokines, also known as chemokines, in the regulation of inflammatory responses per se is now being rapidly expanded to include important functions in control of both early and late phases of the allergic asthmatic response. Central to the importance of chemokines in development and maintenance of allergic asthma is both a direct role in generating local eosinophil accumulation and an ability to influence local events leading to TH2-cell dominance.

This review summarizes recent evidence supporting a continuing role for chemokines and their receptors in the pathogenesis of allergic asthma, and discusses the likely implications of these findings.

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