Oncotarget

Research Papers:

SOCS3 treatment prevents the development of alopecia areata by inhibiting CD8+ T cell-mediated autoimmune destruction

Zhen Gao, Yu-Qing Jin and Wei Wu _

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Oncotarget. 2017; 8:33432-33443. https://doi.org/10.18632/oncotarget.16504

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Abstract

Zhen Gao1, Yu-Qing Jin2, Wei Wu1

1Department of Plastic and Reconstructive Surgery, Shanghai 9th People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China

2Department of Plastic Surgery, Shanghai International Medical Center, Shanghai, China

Correspondence to:

Wei Wu, email: babevivi@126.com

Keywords: alopecia areata, SOCS3, IFN-γ, autoimmune, hair follicle

Received: October 02, 2016    Accepted: February 23, 2017    Published: March 23, 2017

ABSTRACT

Alopecia areata is one of the most common autoimmune diseases resulting from T cell-mediated damage of hair follicles. CD8+ T cells infiltrate hair follicles and are responsible for destruction of hair follicles. However the underlying mechanisms for hair loss remain still obscure. In the present study, we identified that suppressor of cytokine signaling-3 (SOCS3), a classical inhibitor of cytokine signaling, significantly inhibits CD8+T cell maturation, interferon-γ (IFN-γ) production and alopecia areata. SOCS3 is downregulated in the skin of alopecia areata patients and murine autoimmune alopecia model. Furthermore, SOCS3 treatment prevents the development of alopecia areata in the graft model. SOCS3 decreases the CD44high CD62Llow effector memory CD8+ T cells, resulting in the decrease of IFN-γ production. The expression of Fas and major histocompatibility complex-1 (MHC I) is upregulated in skin from C3H/HeJ alopecia areata mice, and this increase is suppressed by SOCS3. The SOCS3 level is negative correlation with the Fas and MHC I level in patients with alopecia areata. These results suggest that SOCS3 treatment may be an effective strategy to treat autoimmune alopecia as well as to more generally prevent cytokine-dependent tissue destruction in inflammatory diseases.


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