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. 2017 Sep;7(3):205-208.
doi: 10.3892/br.2017.952. Epub 2017 Jul 25.

Thymosin β4 in rheumatoid arthritis: Friend or foe

Kyoung Soo Kim  1   2 , Hyung-In Yang  2   3
Affiliations

Thymosin β4 in rheumatoid arthritis: Friend or foe

Kyoung Soo Kim et al. Biomed Rep. 2017 Sep.

Abstract

Rheumatoid arthritis (RA) has characteristic pannus tissues, which show tumor-like growth of the synovium through chronic joint inflammation. The synovium is highly penetrated by various immune cells, and the synovial lining becomes hyperplastic due to increased numbers of macrophage-like and fibroblast-like synoviocytes. Thus, a resultant hypoxic condition stimulates the expression of inflammation-related genes in various cells, in particular, vascular endothelial growth factor. Thymosin β4 (Tβ4), a 5-kDa protein, is known to play a significant role in various biological activities, such as actin sequestering, cell motility, migration, inflammation, and damage repair. Recent studies have provided evidence that Tβ4 may have a role in RA pathogenesis. The Tβ4 level has been shown to increase significantly in the joint fluid and serum of RA patients. However, whether Tβ4 stimulates or inhibits activation of RA immune responses remains to be determined. In the present study, we discuss the logical and clinical justifications for Tβ4 as a potential target for RA therapeutics.

Keywords: angiogenesis; proinflammatory cytokines; rheumatoid arthritis; therapeutic antibody; thymosin β4.

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References

    1. McInnes IB, Schett G. Cytokines in the pathogenesis of rheumatoid arthritis. Nat Rev Immunol. 2007;7:429–442. doi: 10.1038/nri2094. - DOI - PubMed
    1. McInnes IB, Schett G. The pathogenesis of rheumatoid arthritis. N Engl J Med. 2011;365:2205–2219. doi: 10.1056/NEJMra1004965. - DOI - PubMed
    1. Schett G, Elewaut D, McInnes IB, Dayer JM, Neurath MF. How cytokine networks fuel inflammation: Toward a cytokine-based disease taxonomy. Nat Med. 2013;19:822–824. doi: 10.1038/nm.3260. - DOI - PubMed
    1. Kaneko Y, Takeuchi T. A paradigm shift in rheumatoid arthritis over the past decade. Intern Med. 2014;53:1895–1903. doi: 10.2169/internalmedicine.53.2834. - DOI - PubMed
    1. Hyrich KL, Watson KD, Silman AJ, Symmons DP. British Society for Rheumatology Biologics Register: Predictors of response to anti-TNF-alpha therapy among patients with rheumatoid arthritis: Results from the British Society for Rheumatology Biologics Register. Rheumatology (Oxford) 2006;45:1558–1565. doi: 10.1093/rheumatology/kel149. - DOI - PubMed