Posnett David N, Yarilin Dmitry
Immunology Program, Graduate School of Medical Sciences, Weill Medical College, Cornell University, Ithaca, NY, USA.
Arthritis Res Ther. 2005;7(2):74-84. doi: 10.1186/ar1691. Epub 2005 Feb 10.
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.
关于人类自身免疫性疾病中某些慢性持续性微生物(疱疹病毒或衣原体)感染的报告与以下假说相符:这些微生物在免疫缺陷情况下被重新激活,并且常常靶向自身免疫性炎症部位。新的实验动物模型证明了这一原理。一种疱疹病毒或衣原体物种可用于感染诱发短暂自身免疫性疾病的小鼠。这会导致疾病严重程度增加甚至复发。证据表明,这些生物体被特异性地输送到炎症部位并导致进一步的组织破坏,尤其是在宿主免疫抑制时。我们综述了微生物感染放大自身免疫性炎症疾病的证据,这可能是适用于许多人类疾病的一种普遍机制。我们建议,接受免疫抑制药物治疗的自身免疫性疾病患者应能从预防性抗病毒治疗中获益。