Association of Interleukin 1 Family with Systemic Sclerosis
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Association of Interleukin 1 Family with Systemic Sclerosis Li Zhang,1 Jun-Wei Yan,2 Yu-Jie Wang,2 Ya-Nan Wan,2 Bing-Xiang Wang,2 Jin-Hui Tao,3 Bing Chen,4 Bao-Zhu Li,2 Guo-Jun Yang,3 and Jing Wang2,5
Abstract—Systemic sclerosis is a connective tissue disease characterized with fibrosis of skin and/or internal organs, and its specific pathological mechanism remains incompletely understood. IL-1 family, whose biological properties are typically pro-inflammatory and pro-fibrosis, has been associated with systemic sclerosis (SSc). Interleukin (IL)-1 family has 11 members, IL-1α, IL-1β, IL-1Ra, IL-18, IL-33, IL-36α, IL-36β, IL-36γ, IL-36Ra, IL-37, and IL-38. With the exception of IL-1Ra and IL-36Ra, each member has its own receptor signal. Abnormal expression of IL-1 and its potential role in the fibrosis process have been probed earliest, as well as its gene polymorphisms with SSc. IL-33 and IL-18 have also been discussed in the recent years, and IL-33 may contribute to the fibrosis of SSc, while IL-18 remains to be researched to confirm its role in fibrosis process. There is a lack of studies on the association of the other members of the IL-1 family, which might provide us the future study area; much more efforts need to be put on this matter. KEY WORDS: systemic sclerosis; SSc; interleukin 1 family; fibrosis.
INTRODUCTION Systemic sclerosis (SSc; scleroderma) is a connective tissue disease whose pathogenesis is characterized by three hallmarks: fibrosis of the skin and/or internal organs, production of certain autoantibodies, and vasculopathy [1]. The prevailing concept is that SSc starts as a diffuse vasculopathy, followed by immune activation, low-grade inflammation, and subsequent tissue fibrosis. There are two main subtypes of SSc and are defined by the extent of skin involvement: limited cutaneous systemic sclerosis (lcSSc) and diffuse cutaneous systemic sclerosis (dcSSc) [2]. Over the past three decades, there has been an apparent increase Li Zhang and Jun-Wei Yan contributed equally to this work and should be considered co-first authors. 1
Medical Genetics Center, Anhui Medical College, Hefei, China Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, No. 81, Meishan Road, Hefei, Anhui 230032, People’s Republic of China 3 Department of Rheumatology and Immunology, Anhui Provincial Hospital Affiliated to Anhui Medical University, Hefei, China 4 School of Basic Medical Sciences, Anhui Medical University, Hefei, China 5 To whom correspondence should be addressed at Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, No. 81, Meishan Road, Hefei, Anhui 230032, People’s Republic of China. E-mail: [email protected] 2
in the incidence of SSc to approximately 20 per million, possibly due to improved diagnosis. The 7:1 female preponderance of SSc suggested hormonal or pregnancy-related factors might have a role in SSc pathogenesis, but specific pathological mechanism remains incompletely understood [3]. The present studies sug
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