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B2 Is Required for Optimal CD40-Induced IL-12 Production but Dispensable for Th1 Cell Differentiation1
* Department of Pathobiology, University of Pennsylvania, Philadelphia, PA 19104; and
Medical Research Council Center for Immune Regulation, School of Medicine, University of Birmingham, Edgbaston, Birmingham, United Kingdom
NF-
B is a ubiquitously expressed transcription factor involved
in the regulation of innate and adaptive immunity. As part of studies
to define the role of various NF-B family members in Th cell
development and maintenance, we infected NF-B2-/- and
control mice with Leishmania major and followed disease
progression. NF-B2-/- mice on a normally resistant
background develop chronic nonhealing lesions associated with
uncontrolled parasite replication and a failure to develop an IFN-
response. We show that there are no intrinsic defects in Th cell
differentiation in the absence of NF-B2. Indeed,
NF-B2-/- T cells are able to develop a Th1 phenotype
and protect recombination-activating gene-/- mice from
progressive cutaneous leishmaniasis. We demonstrate instead that the
susceptibility of NF-B2-/- mice to L.
major is the result of an IL-12 deficiency, and we provide
evidence for a specific impairment in CD40-induced IL-12 production by
macrophages lacking this transcription factor.
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