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NDT Advance Access originally published online on October 12, 2004
Nephrology Dialysis Transplantation 2004 19(12):2948-2951; doi:10.1093/ndt/gfh497
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Nephrol Dial Transplant Vol. 19 No. 12 © ERA-EDTA 2004; all rights reserved

Editorial Comment

Current paradigms about chemokines as therapeutic targets

Hans-Joachim Anders, Volker Vielhauer and Detlef Schlöndorff

Nephrological Center, Medical Policlinic, Ludwig-Maximilians-University Munich, Germany

Correspondence and offprint requests to: PD Dr H.-J. Anders, Medizinische Poliklinik der LMU, Pettenkoferstr. 8a, 80336 Munich, Germany. Email: hjanders@med.uni-muenchen.de

The first 150 words of the full text of this article appear below.



   Introduction
 
After the recognition of chemotactic cytokines as mediators of inflammation about a decade ago, specific chemokine antagonists are now approaching first clinical trials for non-renal indications [1]. In the field of nephrology, the potential of targeting the chemokine system has also gained much interest. In general, cytokines orchestrate cell–cell communication in order either to maintain tissue homeostasis or to initiate response mechanisms during tissue injury triggered by e.g. trauma, toxicity, immunological insults and infection. Among the cytokines, the chemokines are a distinct group of peptides involved in leukocyte trafficking, which mediate their biological effects through a group of G protein-coupled receptors, the chemokine receptors (CCRs) (reviewed in [2]). In this article we present current paradigms of chemokine biology and indicate future perspectives towards new therapeutic options for the treatment of kidney diseases.



   Paradigm no. 1: some chemokines are involved in tissue homeostasis
 
A subgroup of chemokines within the chemokine family contributes to tissue homeostasis . . . [Full Text of this Article]



   Paradigm no. 2: some chemokines mediate compartment-specific leukocyte recruitment in the initiation phase of renal injury
 


   Paradigm no. 3: infiltrating leukocytes contribute to local chemokine production in the amplification phase of nephritis and bias towards resolution or progression of disease
 


   Paradigm no. 4: non-redundant chemokines or CCR represent therapeutic targets
 


   Paradigm no. 5: inflammatory chemokines have additional immunoregulatory functions
 


   Paradigm no. 6: the chemokine network is species specific
 


   Conclusion
 

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