@Article{,
AUTHOR = {Stéphanie Beq, Jean-François Delfraissy, Jacques Theze},
TITLE = {Interleukin-7 (IL-7): immune function, involvement in the pathogenesis of HIV infection and therapeutic potential},
JOURNAL = {European Cytokine Network},
VOLUME = {15},
YEAR = {2004},
NUMBER = {4},
PAGES = {279--289},
URL = {http://www.techscience.com/ECN/v15n4/66358},
ISSN = {1952-4005},
ABSTRACT = {Interleukin 7 (IL-7), which is constitutively produced particularly by stromal cells from the bone
marrow and thymus, plays a crucial role in T cell homeostasis. This cytokine is implicated in thymopoiesis since
it sustains thymocyte proliferation and survival. It regulates peripheral naive T cell survival by modulating the
expression of the anti-apoptotic molecule Bcl-2, and sustains peripheral T cell expansion in response to antigenic
stimulation. Infection by the human immunodeficiency virus (HIV) leads to severe T lymphopenia and general
immune dysfunction. Increased IL-7 plasma levels are generally observed in HIV-infected patients. The existence
of an inverse correlation between IL-7 plasma levels and the CD4+ T cell count suggests that a direct feedback
mechanism is working to restore peripheral T cell counts in lymphopenic patients. Here, IL-7 plasma levels are
a good predictive marker of CD4+ T cell restoration during therapy. Combinations of antiretroviral treatments
considerably slow disease progression. They drastically decrease the viral load and, in most patients, significantly
increase peripheral CD4+ T cell counts. However, despite their usual ability to reduce viral replication, such
treatments often fail to reverse lymphopenia and do not restore specific antiviral immune responses. IL-7, based
therapy, combined with efficient antiretroviral treatment, may be beneficial to HIV-infected patients by promoting
thymic output, sustaining naive T cell counts and increasing memory T cell activation.},
DOI = {}
}