tailieunhanh - Báo cáo y học: "Amplification of autoimmune disease by infection"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: Amplification of autoimmune disease by infection. | Arthritis Research Therapy Vol 7 No 2 Posnett and Yarilin Review Amplification of autoimmune disease by infection David N Posnett1 2 and Dmitry Yarilin1 2 Immunology Program Graduate School of Medical Sciences Weill Medical College Cornell University Ithaca NY USA 2Department of Medicine Division of Hematology-Oncology Weill Medical College Cornell University Ithaca NY USA Corresponding author David N Posnett dposnett@ Published 10 February 2005 Arthritis Res Ther 2005 7 74-84 DOI ar1691 2005 BioMed Central Ltd Abstract Reports of infection with certain chronic persistent microbes herpesviruses or Chlamydiae in human autoimmune diseases are consistent with the hypothesis that these microbes are reactivated in the setting of immunodeficiency and often target the site of autoimmune inflammation. New experimental animal models demonstrate the principle. A herpesvirus or Chlamydia species can be used to infect mice with induced transient autoimmune diseases. This results in increased disease severity and even relapse. The evidence suggests that the organisms are specifically imported to the inflammatory sites and cause further tissue destruction especially when the host is immunosuppressed. We review the evidence for the amplification of autoimmune inflammatory disease by microbial infection which may be a general mechanism applicable to many human diseases. We suggest that patients with autoimmune disorders receiving immunosuppressing drugs should benefit from preventive antiviral therapy. What do herpesviruses Chlamydiae and parvovirus B19 have in common The question of how infectious organisms contribute to autoimmunity has continued to be of interest to clinical rheumatologists and basic immunologists. Recent reviews have considered the possible contributions of different non-mutually exclusive mechanisms including molecular mimicry bystander activation cryptic antigens and epitope spreading 1-3 . However current understanding as .

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