The chemokine family is responsible for the specific, specialized trafficking of leukocytes.
Inflammation is characterized by an excessive, inappropriate cellular recruitment.
Chemokine receptors are necessary for HIV infection.
The large number of chemokines and receptors point to a redundant system. In vitro studies support this, but in vivo studies provide evidence for specificity in the chemokine system.
Clinical evidence shows that chemokines and receptors are expressed abundantly in samples and biopsies from patients suffering from inflammatory disorders.
Patients that lack CCR5 are resistant to HIV infection.
Studies using gene-deleted mice, neutralization of ligands or receptors and small molecule inhibitors have all contributed to our understanding of the chemokine system.
Chemokine receptors are valid therapeutic targets for the treatment of inflammation and HIV infection.
Chemokines and their receptors are involved in the pathogenesis of diseases ranging from asthma to AIDS. Chemokine receptors are G-protein-coupled serpentine receptors that present attractive tractable targets for the pharmaceutical industry. It is only ten years since the first chemokine receptor was discovered, and the rapidly expanding number of antagonists holds promise for new medicines to combat diseases that are currently incurable. Here, I focus on the rationale for developing antagonists of chemokine receptors for inflammatory disorders and AIDS, and the accumulating evidence that favours this strategy despite the apparent redundancy in the chemokine system.