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*
Clinical Immunology Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases; and
National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892
IFN-
exerts multiple biological activities in the modulation of
immune responses by the induction of transcription factors. One
transcriptional factor of the IFN regulatory factor family found to be
critical in regulating IL-12-dependent IFN- production in vivo
following infectious challenge has been designated IFN consensus
sequence-binding protein (ICSBP). In this study, the role of ICSBP in
regulating type 1 responses to T cell-specific stimulation in vitro was
assessed. Total splenocytes from ICSBP-/- mice stimulated
with soluble anti-CD3 were markedly impaired in the production of
IFN- compared with similarly stimulated cells from
ICSBP+/+ mice. Consistent with the decrease in IFN-
production, splenocytes from ICSBP-/- mice stimulated
with anti-CD3 in the presence or absence of IFN- or a soluble
CD40 ligand agonist failed to produce IL-12 p40 and IL-12 p70 protein;
however, the deficient production of IFN- from
ICSBP-/- mice could be restored by the addition of
anti-CD28 Ab in an IL-12-independent manner. In contrast to the
previous data, production of IFN- from naive
CD4+/LECAM-1high cells of
ICSBP-/- mice that had been primed in vitro with
anti-CD3 was similar to or greater than that of
ICSBP+/+ controls. In addition, the presence of IFN- in
priming cultures enhanced both priming for IFN- and IL-12
responsiveness from ICSBP-/- CD4+ T cells.
Overall, these results provide evidence that ICSBP is differentially
required for the ability of IFN- to regulate type 1 cytokine
responses from APCs and CD4+ T cells.
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