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The immunobiology of viral arthritides

期刊

PHARMACOLOGY & THERAPEUTICS
卷 124, 期 3, 页码 301-308

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pharmthera.2009.09.005

关键词

Viral arthritides; Chikungunya virus; Ross River virus; Cytokines; Chemokines; Macrophage; Inflammation; Monocyte chemoattractant protein-1

资金

  1. Australian National Health
  2. Medical Research Council
  3. NHMRC Principal Research Fellowship
  4. Australian NHMRC R. Douglas Wright Fellowship

向作者/读者索取更多资源

A large range of human viruses are associated with the development of arthritis or arthralgia. Although there are many parallels with autoimmune arthritides, there is little evidence that viral arthritides lead to autoimmune disease. in humans viral arthritides usually last from weeks to months, can be debilitating, and are usually treated with non-steroidal anti-inflammatory drugs, but with variable success. Viral arthritides likely arise from immunopathological inflammatory responses directed at viruses and/or their products residing and/or replicating within joint tissues. Macrophages recruited by monocyte chemoattractant protein-1 (MCP-1/CCL2) and activated by interferon, and proinflammatory mediators like turnout necrosis factor alpha, interferon gamma, interleukin-6 and interieukin-1 beta appear to be common elements in this group of diseases. The challenge for new treatments is to target excessive inflammation without compromising antiviral immunity. Recent evidence from mouse models suggests targeting MCP-1 or complement may emerge as viable new treatment options for viral arthritides. (C) 2009 Published by Elsevier Inc.

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