Biologic treatment in Sjogren's syndrome

被引:51
作者
Sada, Pablo Ruiz [1 ]
Isenberg, David [2 ]
Ciurtin, Coziana [3 ]
机构
[1] Hosp Univ Basurto, Dept Med Interna, Bilbao, Spain
[2] UCL, Ctr Rheumatol Res, Div Med, London NW1 2PG, England
[3] UCL, Dept Rheumatol, London NW1 2PG, England
关键词
Sjogren's syndrome; biologic therapies; B cell-targeted therapy; rituximab; belimumab; epratuzumab; T cell modulation therapy; abatacept; interferon; HUMANIZED ANTI-CD22 ANTIBODY; PLACEBO-CONTROLLED TRIAL; GLAND TISSUE EXPRESSION; CELL-ACTIVATING FACTOR; BAFF TRANSGENIC MICE; LONG-TERM EFFICACY; ZONE B-CELLS; DOUBLE-BLIND; RITUXIMAB TREATMENT; CLINICAL-TRIAL;
D O I
10.1093/rheumatology/keu417
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
SS is a chronic systemic autoimmune disease characterized by decreased exocrine gland function. A variety of other disease manifestations may also be present, including general constitutional symptoms and extraglandular features. A multidisciplinary approach focused on both local and systemic medical therapies is needed as the disease has a wide clinical spectrum. The current treatment for SS is mainly symptomatic. However, there is evidence that systemic drugs are effective in controlling extraglandular manifestations of the disease. Overall evidence for the role of conventional immunosuppressive therapy is limited. A number of attempts to use biologic therapies have led to variable results. Biologic agents targeting B cells, such as rituximab, epratuzumab and belimumab, have shown promising results, but further studies are needed to validate the findings. Early-phase studies with abatacept and alefacept proved that T cell stimulation inhibition is another potentially effective target for SS treatment. Modulation or inhibition of other targets such as IFN, IL-6 and Toll-like receptor are also currently being investigated. We have summarized the available evidence regarding the efficacy of biologic treatments and discuss other potential therapies targeting pathways or molecules recognized as being involved in the pathogenesis of SS.
引用
收藏
页码:219 / 230
页数:12
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