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B Family Members in Control of Helminth Infection and Intestinal Inflammation1
* Department of Pathobiology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA 19104;
Medical Research Council Center for Immune Regulation, School of Medicine, University of Birmingham, Birmingham, United Kingdom; and
Department of Medicine, Division of Immunology, Cornell University Medical College, New York, NY 10021
The NF-
B family of transcription factors is critical in
controlling the expression of a wide range of immune response genes.
However, whether individual family members perform specific roles in
regulating immunity and inflammation remains unclear. Here we
investigated the requirement for NF-B1, NF-B2, and c-Rel in the
expression of Th2 cytokine responses, development of host protective
immunity, and regulation of intestinal inflammation following infection
with the gut-dwelling helminth parasite Trichuris muris.
While mice deficient in c-Rel mounted sufficient Th2 responses to expel
infection, NF-B1 knockout (KO) and NF-B2 KO mice developed
chronic infections associated with elevated production of Ag-specific
IFN-
. However, only infected NF-B1 KO mice exhibited polarized
IFN- responses associated with the loss of intestinal goblet cells
and the development of destructive colitis-like pathology. Furthermore,
blockade of IL-12 (previously shown to confer resistance in susceptible
strains) recovered Ag-specific IL-13 responses and resistance to
infection in NF-B2 KO, but not NF-B1 KO mice. Therefore, unique
infection, immunological, and pathological outcomes were observed in
different NF-B KO strains. Taken together, these results
provide direct evidence of nonoverlapping functions for NF-B
family members in the development of Th2 cytokine-mediated resistance
to T. muris and the control of infection-induced
intestinal inflammation.
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