Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 16, Issue 1, Pages 887-906Publisher
MDPI
DOI: 10.3390/ijms16010887
Keywords
autoimmunity; arthritis; biologics; cytokines; gene therapy; inflammation; interleukins; rheumatoid arthritis; siRNA
Funding
- National Institutes of Health (NIH)/NCCAM, Bethesda, MD, USA [R01AT004321]
- NATIONAL CENTER FOR COMPLEMENTARY & ALTERNATIVE MEDICINE [R01AT004321] Funding Source: NIH RePORTER
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Cytokines are the key mediators of inflammation in the course of autoimmune arthritis and other immune-mediated diseases. Uncontrolled production of the pro-inflammatory cytokines such as interferon-gamma (IFN-gamma), tumor necrosis factor a (TNF alpha), interleukin-6 (IL-6), and IL-17 can promote autoimmune pathology, whereas anti-inflammatory cytokines including IL-4, IL-10, and IL-27 can help control inflammation and tissue damage. The pro-inflammatory cytokines are the prime targets of the strategies to control rheumatoid arthritis (RA). For example, the neutralization of TNF alpha, either by engineered anti-cytokine antibodies or by soluble cytokine receptors as decoys, has proven successful in the treatment of RA. The activity of pro-inflammatory cytokines can also be downregulated either by using specific siRNA to inhibit the expression of a particular cytokine or by using small molecule inhibitors of cytokine signaling. Furthermore, the use of anti-inflammatory cytokines or cytokine antagonists delivered via gene therapy has proven to be an effective approach to regulate autoimmunity. Unexpectedly, under certain conditions, TNF alpha, IFN-gamma, and few other cytokines can display anti-inflammatory activities. Increasing awareness of this phenomenon might help develop appropriate regimens to harness or avoid this effect. Furthermore, the relatively newer cytokines such as IL-32, IL-34 and IL-35 are being investigated for their potential role in the pathogenesis and treatment of arthritis.
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