Kiazyk Sandra A Koesters, Fowke Keith R
Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba R3E 0W3, Canada.
Trends Microbiol. 2008 Dec;16(12):567-73. doi: 10.1016/j.tim.2008.08.011. Epub 2008 Oct 27.
Although chronic immune activation correlates with CD4(+) T cell loss in HIV infection, an understanding of the factors mediating T cell depletion remains incomplete. We propose that reduced expression of CD127 (IL-7 receptor alpha chain, IL-7Ralpha), induced by immune activation, contributes to CD4(+) T cell loss in HIV infection. In particular, loss of CD127 on central memory CD4(+) T cells (T(CM)) severely restrains the regenerative capacity of the memory component of the immune system, resulting in a limited ability to control T cell homeostasis. Studies from both pathogenic and controlled HIV infection indicate that the containment of immune activation and preservation of CD127 expression are critical to the stability of CD4(+) T cells in infection. A better understanding of the factors regulating CD127 expression in HIV disease, particularly on T(CM) cells, might unveil new approaches exploiting the IL-7/IL-7R receptor pathway to restore T cell homeostasis and promote immune reconstitution in HIV infection.
尽管慢性免疫激活与HIV感染中CD4(+) T细胞的丧失相关，但对介导T细胞耗竭的因素的理解仍不完整。我们提出，免疫激活诱导的CD127（白细胞介素-7受体α链，IL-7Rα）表达降低，促成了HIV感染中CD4(+) T细胞的丧失。特别是，中央记忆CD4(+) T细胞（T(CM)）上CD127的丧失严重限制了免疫系统记忆成分的再生能力，导致控制T细胞稳态的能力有限。来自致病性和可控性HIV感染的研究表明，抑制免疫激活和保留CD127表达对于感染中CD4(+) T细胞的稳定性至关重要。更好地理解HIV疾病中调节CD127表达的因素，尤其是在T(CM)细胞上的因素，可能会揭示利用白细胞介素-7/白细胞介素-7受体途径来恢复T细胞稳态并促进HIV感染中免疫重建的新方法。
