Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Editorial
. 2018 Jun;70(6):801-804.
doi: 10.1002/art.40445. Epub 2018 May 2.

Editorial: STATus of STAT3 in Psoriatic Arthritis

John D Mountz  1
Affiliations
Editorial

Editorial: STATus of STAT3 in Psoriatic Arthritis

John D Mountz. Arthritis Rheumatol. 2018 Jun.
No abstract available

PubMed Disclaimer

Figures

Figure 1
Figure 1. STAT3 in CD4 T cells promote psoriasis and psoriatic arthritis
The article by Ding and colleagues in the current issue shows that constitutive hyperexpression of STAT3 in mouse CD4+ T cells is sufficient to promote psoriasis-like skin disease, psoriasis-like arthritis and enthesopathy. Taken together with other data, the results suggest a model in which constitutive expression of STAT3, with or without IL-6 signaling, promotes an inflammatory environment including IL-1, TGFβ and IL-23 that promotes development and differentiation of Th17 cells (upper pathway). The same conditions in the presence of TNFα and IL-23 lead to the sustained development of Th22 T cells (lower pathway). Th17 cells express characteristic transcription factors, STAT3 and RORᵧt; chemokine receptors, CCR4 and CCR6; and cytokines IL-17a, IL-17f, IL-22 and IL-21. Collectively, these promote development of a psoriasis-like arthritis and individuals with higher STAT3 transcriptional activity are more susceptible to joint disease (upper pathway). Th22 cells express canonical transcription factors, STAT3, NF-kB and aryl hydrocarbon receptor (AhR); chemokine receptors, CCR4, CCR6 and CCR10; and cytokines, IL-22, TNF, IL-13 and IL-26. Collectively, these promote development of skin psoriasis and individuals with high STAT3 transcriptional activity are more likely to develop skin disease (lower pathway).
See this image and copyright information in PMC

Comment on

References

    1. Sano S, et al. Stat3 links activated keratinocytes and immunocytes required for development of psoriasis in a novel transgenic mouse model. Nat Med. 2005;11(1):43–9. - PubMed
    1. Yamamoto M, et al. Psoriatic inflammation facilitates the onset of arthritis in a mouse model. J Invest Dermatol. 2015;135(2):445–453. - PubMed
    1. Yang La, K SB. Augmented Th17 Differentiation Leads to Cutaneous and Synovio-Entheseal Inflammation in a Novel Model of Psoriatic Arthritis. Arthritis & Rheumatology. 2018 - PMC - PubMed
    1. Bromberg JF, et al. Stat3 as an oncogene. Cell. 1999;98(3):295–303. - PubMed
    1. Maritano D, et al. The STAT3 isoforms alpha and beta have unique and specific functions. Nat Immunol. 2004;5(4):401–9. - PubMed

Publication types

Substances