Abstract
In summary, experimental and clinical studies in the last few years have shown that renal tissues produce chemokines in response to stimulation by proinflammatory cytokines, immune complexes, complement activation, vasoactive peptides, and hypoxia. These tissue insults lead to a transient increase in chemokines. This increase initiates the recruitment of inflammatory cells, and probably starts the auto-induction loop of transforming growth factor-β, which may mediate tissue fibrogenesis. The development of neutralizing humanized antibodies against chemokines or the development of nonsignaling receptor antagonists may offer therapeutic opportunities in the treatment of renal injuries or transplant rejection.
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