Yu Sheng-Jie, Liao En-Chih, Tsai Jaw-Ji
Institute of Biomedical Sciences, National Chung Hsing University, Taichung, Taiwan.
Center for Translational Medicine, Department of Medical Research, Taichung Veterans General Hospital; Department of BioIndustry Technology, Da Yeh University, Changhua, Taiwan; Department of Medical Technology, Jen Ten College of Medicine, Nursing and Management, Miaoli, Taiwan.
Immunobiology. 2014 Dec;219(12):958-63. doi: 10.1016/j.imbio.2014.07.018. Epub 2014 Aug 4.
Although many patients with SLE also have allergies, the immunological events triggering the onset and progression of the clinical manifestations of SLE by allergens have yet to be clarified. A total of three autoantigens, phosphoglycerate kinase 1 (PGK-1), triosephosphate isomerase (TIM) and enolase were identified by autologous serum in B cell lysate derived from HDM allergic SLE patients after Der p 2 stimulation. Autoantigen, TRIM-21 expression were also significantly increased in B cells derived from HDM allergic SLE patients. In PBMCs derived from SLE patients, the concentration of anti-PGK-1 was significantly upregulated after Der p 2 stimulation compared to HDM allergic without SLE patients and healthy subjects. Inflammatory related cytokines and chemokines include IL-1β, IL-6, IL-8, CXCL5 could be upregulated after Der p 2 stimulation in PBMCs derived from HDM allergic SLE patients. In conclusion, our data demonstrated that long-term allergen exposure could be a contributing factor in the development of SLE.