Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rm 6146, 50 South Drive, Bethesda, Maryland, 20892, USA.
Nat Rev Microbiol. 2012 Jan 9;10(2):150-6. doi: 10.1038/nrmicro2712.
Some individuals who are infected with HIV rapidly deteriorate shortly after starting antiretroviral therapy, despite effective viral suppression. This reaction, referred to as immune reconstitution inflammatory syndrome (IRIS), is characterized by tissue-destructive inflammation and arises as CD4(+) T cells re-emerge. It has been proposed that IRIS is caused by a dysregulation of the expanding population of CD4(+) T cells specific for a co-infecting opportunistic pathogen. Here, we argue that IRIS instead results from hyper-responsiveness of the innate immune system to T cell help, a mechanism that may be shared by the many manifestations of IRIS that occur following the reversal of other types of immunosuppression in pathogen-infected hosts.
有些感染 HIV 的个体在开始抗逆转录病毒治疗后不久，尽管病毒得到有效抑制，仍会迅速恶化。这种反应被称为免疫重建炎症综合征（IRIS），其特征是组织破坏性炎症，并且随着 CD4(+)T 细胞的重新出现而出现。有人提出，IRIS 是由针对合并感染机会性病原体的 CD4(+)T 细胞的扩张群体的失调引起的。在这里，我们认为 IRIS 是由先天免疫系统对 T 细胞辅助的过度反应引起的，这种机制可能与感染宿主中其他类型免疫抑制逆转后发生的许多 IRIS 表现共享。
