@Article{ecn.2010.0206,
AUTHOR = {François Villinger, Aftab A. Ansari},
TITLE = {Role of IL-12 in HIV infection and vaccine},
JOURNAL = {European Cytokine Network},
VOLUME = {21},
YEAR = {2010},
NUMBER = {3},
PAGES = {215--218},
URL = {http://www.techscience.com/ECN/v21n3/65861},
ISSN = {1952-4005},
ABSTRACT = {Among cytokines that dictate the fate of developing immune responses, IL-12 represents an
important nexus for the development of type I cell-mediated immune responses (CMI). This factor is primarily
produced by monocytic cell lineages in response to stimuli such as pathogen-associated molecular patterns, dic-tating
the development of naive T cells as they differentiate into antigen-specific T cells. HIV infection results in
an early loss of effective TH1 prototype CMI when such responses appear to be precisely the type of CMI
needed to control the virus and a host of opportunistic pathogens. Besides CD4 T cell loss, much of the muted
IL-12 response has been attributed to direct effects of HIV or its proteins on antigen-presenting cells, while T
and NK cell responses to IL-12 appear maintained during chronic HIV infection. However, while IL-12 therapy
is unlikely to provide major benefits in the context of an established HIV infection, IL-12 preconditioning of
monkeys during acute SIV infection markedly delayed disease progression. These findings suggest that IL-12
may serve as a critical vaccine adjuvant, and as treatment for particular opportunistic agents or neoplasm
such as Kaposi’s sarcoma; it has already shown promising results in the context of HIV infection.},
DOI = {10.1684/ecn.2010.0206}
}