期刊
JOURNAL OF IMMUNOLOGY
卷 168, 期 9, 页码 4406-4413出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.168.9.4406
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资金
- NIAID NIH HHS [AI-41880, AI-35914, AI-0752, AI-41158] Funding Source: Medline
NF-kappaB 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-kappaB family members in Th cell development and maintenance, we infected NF-kappaB2(-/-) and control mice with Leishmania major and followed disease progression. NF-kappaB2(-/-) mice on a normally resistant background develop chronic nonhealing lesions associated with uncontrolled parasite replication and a failure to develop an IFN-gamma response. We show that there are no intrinsic defects in Th cell differentiation in the absence of NF-kappaB2. Indeed, NF-kappaB2(-/-) 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-kappaB2(-/-) 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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