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CCR6 and CCL20: emerging players in the pathogenesis of rheumatoid arthritis

Adrian Y S Lee1, Heinrich Körner2

  • 11] Menzies Research Institute Tasmania, University of Tasmania, Hobart, Tasmania, Australia [2] School of Medicine, University of Tasmania, Hobart, Tasmania, Australia.

Immunology and Cell Biology
|January 8, 2014
PubMed

Insights

Targeting C-C chemokine ligand CCL20 and its receptor CCR6 offers a promising new approach for rheumatoid arthritis (RA) treatment, addressing limitations of current therapies like anti-TNF agents.

Area of Science:

  • Immunology
  • Rheumatology
  • Molecular Biology

Background:

  • Current treatments for chronic inflammatory diseases, such as anti-TNF biologics and methotrexate, have limitations including side effects and therapy resistance.
  • Targeting chemokine pathways presents a novel therapeutic strategy to specifically disrupt immune cell migration in inflammatory diseases.

Purpose of the Study:

  • To explore the genetic and biological role of C-C chemokine ligand 20 (CCL20) and its receptor C-C chemokine receptor 6 (CCR6) in rheumatoid arthritis (RA).
  • To evaluate CCR6 as a potential therapeutic target for RA, considering its expression patterns and association with the disease.

Main Methods:

  • Review of genetic association studies, including genome-wide association studies (GWAS), implicating CCR6 in RA pathogenesis.
  • Analysis of CCL20 and CCR6 expression patterns within RA tissues and the immune system.

Main Results:

  • Genome-wide association studies have identified a significant association between CCR6 and RA.
  • Expression patterns of CCL20 and CCR6 suggest their involvement in immune cell infiltration and inflammatory processes in RA.

Conclusions:

  • The CCL20-CCR6 axis is a compelling target for developing novel, specialized therapies for rheumatoid arthritis.
  • Targeting this pathway may overcome the limitations of existing treatments by specifically modulating immune cell trafficking in RA.

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