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Prepublished online as a Blood First Edition Paper on June 28, 2002; DOI 10.1182/blood-2002-04-1088.
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Blood, 1 January 2003, Vol. 101, No. 1, pp. 305-310
PHAGOCYTES
Essential role for ICSBP in the in vivo development of murine
CD8 + dendritic cells
Julio Aliberti,
Oliver Schulz,
Daniel J. Pennington,
Hideki Tsujimura,
Caetano Reis e
Sousa,
Keiko Ozato, and
Alan Sher
From the Immunobiology Section, Laboratory of Parasitic
Diseases, National Institute of Allergy and Infectious Diseases
(NIAID), and Laboratory of Molecular Growth Regulation, National
Institute of Child Health and Human Development (NICHD), National
Institutes of Health, Bethesda, MD; and Immunobiology and Lymphocyte
Molecular Biology Laboratories, Cancer Research United Kingdom, London
Research Institute, London, United Kingdom.
Interferon (IFN) consensus sequence-binding protein (ICSBP) is an
important transcription factor regulating proinflammatory cytokine
production and the development of mononuclear phagocytes in vitro. Here
we analyzed the role of ICSBP in the in vivo differentiation of 3 major
subsets of murine dendritic cells (DCs). We found that ICSBP is
predominantly expressed by the CD8 + subset, and more
important, that ICSBP / mice have a profound and
selective deficiency in CD8+ DEC205+ DCs in
lymphoid tissues. Studies using wild-type/ICSBP/
chimeras revealed that this defect in CD8+ DC
development is intrinsic to bone marrow-derived progenitors and not
dependent on ICSBP expression in the nonhemopoietic compartment. Because DC precursor frequencies are unaltered in the bone marrow of
ICSBP/ mice, ICSBP appears to function by regulating
CD8+ DC differentiation downstream from the generation
of common DC progenitors. Although CD8 DCs are present
in normal numbers in ICSBP/ animals, up-regulation of
CD40, CD80, and major histocompatibility complex (MHC) class II
expression was found to be impaired in this subset after in vivo
microbial stimulation. Together these results demonstrate that ICSBP is
critically required for the in vivo differentiation of
CD8+ DCs and may also influence the functional
maturation of the CD8 subsets.
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