Eur J Immunol. 1999 Jul;29(7):2309-18. Unique Identifier : AIDSLINE
Dendritic cells (DC) in HIV-1 infection show a reduced capacity to
stimulate primary T cell proliferation. Exposure of bone marrow-derived
DC to Rauscher leukemia virus (RLV) provides a mouse model for studying
retrovirally induced reduction in stimulatory capacity for T cells.
Treatment with IL-12, a cytokine that promotes the development of Th1
cells, has been postulated as a treatment for AIDS and is effective at
restoring cell-mediated immunity in mice infected with mouse AIDS virus
or with RLV (see Knight, S. C. and Patterson, S., Annu. Rev. Immunol.
1994. 15: 593-615 for references). Here we studied the direct effect of
RLV and of IL-12 on bone marrow-derived DC. Normal DC produced IL-12 and
IL-10 and stimulated primary allogeneic T cell proliferation. Exposure
of DC to RLV caused reduced production of IL-12, production of IL-4 was
seen in DC for the first time and T cell stimulation was inhibited.
Addition of IL-12 reinstated and enhanced IL-12 synthesis in RLV-treated
DC, abrogated production of IL-10 and IL-4 and restored stimulatory
activity. Manipulation of cytokine production in DC could be a stratagem
that has evolved in the retrovirus to avoid stimulation of cellular
JOURNAL ARTICLE Animal Base Sequence Dendritic Cells/*IMMUNOLOGY DNA
Primers/GENETICS DNA, Viral/GENETICS/ISOLATION & PURIF Human HIV
Infections/IMMUNOLOGY HIV-1 Immune Tolerance In Vitro
Interleukin-12/*BIOSYNTHESIS Interleukin-4/*BIOSYNTHESIS Lymphocyte
Transformation Mice Mice, Inbred BALB C Mice, Inbred CBA Rauscher
Virus/GENETICS/*IMMUNOLOGY/PATHOGENICITY Th1 Cells/IMMUNOLOGY Th2