Sexual dimorphism in autoimmunity: a focus on Th1/Th2 cytokines and multiple sclerosis |
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| Affiliation: | 1. Department of Surgery, Seoul St. Mary''s Hospital, Seoul, Republic of Korea;2. Department of Surgery, Bucheon St. Mary''s Hospital, Gyeonggi, Republic of Korea;3. Department of Surgery, Daejeon St. Mary''s Hospital, Daejeon, Republic of Korea;4. Department of Surgery, Incheon St. Mary''s Hospital, Incheon, Republic of Korea;5. Department of Surgery, Uijeongbu St. Mary''s Hospital, Gyeonggi, Republic of Korea;6. Department of Surgery, Yeouido St. Mary''s Hospital, The Catholic University of Korea, Seoul, Republic of Korea;1. Center for Imaging of Neurodegenerative Diseases, San Francisco Veterans Affairs Medical Center, 4150 Clement Street, 114M, San Francisco, CA 94121, United States;2. Department of Radiology and Biomedical Imaging, University of California San Francisco, San Francisco, CA, United States;3. Department of Psychiatry, University of California San Francisco, San Francisco, CA, United States;1. School of Ophthalmology & Optometry, The Eye Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China;2. State Key Laboratory Cultivation Base and Key Laboratory of Vision Science, Ministry of Health of the People’s Republic of China, Zhejiang Provincial Key Laboratory of Ophthalmology and Optometry, Wenzhou, Zhejiang, China;1. School of Chemical Engineering and Technology, Hebei University of Technology, Tianjin 300130, China;2. National Key Laboratory of Biochemical Engineering, Institute of Process Engineering, Chinese Academy of Science, Beijing 100190, China;3. Collaborative Innovation Center of Chemical Science and Engineering (Tianjin), Tianjin 300072, China;1. Department of Cardiology, University Medical Center Groningen, University of Groningen, RB Groningen, the Netherlands;2. Cardiovascular Translational Research, Sanataria de Navarra Research Institute, Pamplona, Spain;1. Department of General Internal Medicine, Kobe City Medical Center General Hospital, Hyogo, Japan;2. Department of Pathology, Kobe City Medical Center General Hospital, Hyogo, Japan |
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| Abstract: | Many autoimmune diseases preferentially affect women. The underlying reasons for this gender bias are not clear, but are thought to relate to the effects of sex hormones on the immune system. Here we define many of the immune response differences between the genders that may contribute to the increased incidence of MS in females. There is extensive evidence that women respond more vigorously to immune stimuli than men. Increased inflammatory or Th1 cytokine secretion vs. regulatory or Th2 cytokine secretion in females could cause women with MS to have exaggerated immune reactions compared to men. Our previous studies and our preliminary data show that MS patients have a higher number of IFNγ secreting T cells in response to proteolipid protein (PLP) and that this appears to be strongly skewed toward MS females. We hypothesize that this elevated IFNγ response is due to increased IL-12 secretion in females, which has been suggested in animal models of MS. Since induction of IL-12 by antigen is costimulation dependent, we also propose that expression of costimulatory molecules has a strong likelihood of showing gender-specific upregulation. Here we review some of the controversy surrounding the role of sex hormones in regulating the immune response. One of our goals is to help define the role of sex hormones in promoting or suppressing autoimmune responses in MS. Ultimately, understanding the effect that gender plays in the Th1/Th2 cytokine balance in MS patients may allow development of new therapies that capitalize on the different immunological responses in women versus men. |
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