TY - JOUR
T1 - Antiviral immune responses
T2 - Triggers of or triggered by autoimmunity?
AU - Münz, Christian
AU - Lünemann, Jan D.
AU - Getts, Meghann Teague
AU - Miller, Stephen D.
N1 - Funding Information:
The laboratory of C.M. is supported by the Dana Foundation’s Neuroimmunology programme, the Arnold and Mabel Beckman Foundation, the Alexandrine and Alexander Sinsheimer Foundation, the Burroughs Wellcome Fund, the Starr Foundation, the National Cancer Institute (R01CA108609 and R01CA101741), the National Institute of Allergy and Infectious Diseases (RFP-NIH-NIAID-DAIDS-BAA-06-19), the Foundation for the National Institutes of Health (Grand Challenges in Global Health) and an Institutional Clinical and Translational Science Award (to the Rockefeller University Hospital). J.D.L. is supported by a Dana Foundation and Irvington Institute’s Human Immunology Fellowship, a Pilot Grant from the National Multiple Sclerosis Society (PP1145) and an Institutional Clinical and Translational Science Pilot and Collaborative Project Grant (to the Rockefeller University Hospital). The laboratory of S.D.M. and M.T.G. is supported by the National Institute for Neurological Diseases and Stroke (R01 NS-023349, R01 NS-040460 and R01 NS-030871), the National Multiple Sclerosis Society (RG 3793-A-7) and the Myelin Repair Foundation.
PY - 2009/4
Y1 - 2009/4
N2 - The predisposition of individuals to several common autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus and multiple sclerosis, is genetically linked to certain human MHC class II molecules and other immune modulators. However, genetic predisposition is only one risk factor for the development of these diseases, and low concordance rates in monozygotic twins, as well as the geographical distribution of disease risk, suggest the involvement of environmental factors in the development of these diseases. Among these environmental factors, infections have been implicated in the onset and/or promotion of autoimmunity. In this Review, we outline the mechanisms by which viral infection can trigger autoimmune disease and describe the pathways by which infection and immune control of infectious disease might be dysregulated during autoimmunity.
AB - The predisposition of individuals to several common autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus and multiple sclerosis, is genetically linked to certain human MHC class II molecules and other immune modulators. However, genetic predisposition is only one risk factor for the development of these diseases, and low concordance rates in monozygotic twins, as well as the geographical distribution of disease risk, suggest the involvement of environmental factors in the development of these diseases. Among these environmental factors, infections have been implicated in the onset and/or promotion of autoimmunity. In this Review, we outline the mechanisms by which viral infection can trigger autoimmune disease and describe the pathways by which infection and immune control of infectious disease might be dysregulated during autoimmunity.
UR - http://www.scopus.com/inward/record.url?scp=63149158618&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=63149158618&partnerID=8YFLogxK
U2 - 10.1038/nri2527
DO - 10.1038/nri2527
M3 - Review article
C2 - 19319143
AN - SCOPUS:63149158618
SN - 1474-1733
VL - 9
SP - 246
EP - 258
JO - Nature Reviews Immunology
JF - Nature Reviews Immunology
IS - 4
ER -
