Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 203, Issue 2, Pages 449-459Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20051866
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Funding
- NIAID NIH HHS [R01 AI040310-09, R01 AI040310, AI40310, R29 AI040310] Funding Source: Medline
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The major histocompatibility complex (MHC) class Ib molecule H2-M3 primes the rapid expansion of CD8(+) T cells by presenting N-formylated bacterial peptides. However, the significance of H2-M3-restricted T cells in host defense against bacteria is unclear. We generated H2-M3-deficient mice to investigate the role of H2-M3 in immunity against Listeria monocytogenes (LM), a model intracellular bacterial pathogen. H2-M3-deficient mice are impaired in early bacterial clearance during primary infection, with diminished LM-specific CD8(+) T cell responses and compromised innate immune functions. Although H2-M3-restricted CD8(+) T cells constitute a significant proportion of the anti-listerial CD8(+) T cell repertoire, the kinetics and magnitude of MHC class Ia-restricted T cell responses are not altered in H2-M3-deficient mice. The fact that MHC class Ia-restricted responses cannot compensate for the H2-M3-mediated immunity suggests a nonredundant role of H2-M3 in the protective immunity against LM. Thus, the early H2-M3-restricted response temporally bridges the gap between innate and adaptive immune responses, subsequently affecting the function of both branches of the immune system.
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