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The Journal of Immunology, 2001, 166: 6776-6783.
Copyright © 2001 by The American Association of Immunologists

BALB/c Mice Bearing a Transgenic IL-12 Receptor {beta}2 Gene Exhibit a Nonhealing Phenotype to Leishmania major Infection Despite Intact IL-12 Signaling

Ryuta Nishikomori*, Sanjay Gurunathan{dagger}, Kanako Nishikomori* and Warren Strober1,*

* Mucosal Immunity Section and {dagger} Clinical Immunology Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892

In BALB/c mice infected with Leishmania major, early secretion of IL-4 leads to a Th2-type response and nonhealing. We explored the role of IL-4-induced down-regulation of the IL-12R{beta}2 chain in the establishment of this Th2 response. First, we showed that the draining lymph nodes of resistant C57BL/6 mice infected with L. major were enriched in CD4+/IL-12R{beta}2 chain+ cells producing IFN-{gamma}. Next, we demonstrated that BALB/c background mice bearing an IL-12R{beta}2-chain transgene manifested a nonhealing phenotype similar to wild-type littermates despite the persistence of their ability to undergo STAT4 activation. Finally, we found that such transgenic mice display more severe infection than wild-type littermates when treated with IL-12 7 days after infection, and under this condition, the mice display increased Leishmania Ag-induced IL-4 secretion. These studies indicate that although CD4+/IL-12R{beta}2 chain+ T cells are important components of the Th1 response, maintenance of IL-12R{beta}2 chain expression is not sufficient to change a Th2 response to a Th1 response in vivo and thus to allow BALB/c mice to heal L. major infection.




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