Loss of CD127 expression links immune activation and CD4(+) T cell loss in HIV infection.
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.
Kiazyk
Sandra A Koesters
SA
Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba R3E 0W3, Canada.
Fowke
Keith R
KR
D018791:CD4 Lymphocyte Count; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D015536:Down-Regulation; D015658:HIV Infections / Q000276:immunology* / Q000821:virology; D015497:HIV-1 / Q000276:immunology*; D006706:Homeostasis; D006801:Humans; D007156:Immunologic Memory; D053699:Interleukin-7 Receptor alpha Subunit / Q000235:genetics / Q000378:metabolism*; D008213:Lymphocyte Activation
D053699:Interleukin-7 Receptor alpha Subunit