Article

Cross-Recognition of N-Formylmethionine Peptides Is a General Characteristic of H2-M3-Restricted CD8+ T Cells

Cornell University, Итак, New York, United States
Infection and Immunity (Impact Factor: 3.73). 08/2005; 73(7):4423-6. DOI: 10.1128/IAI.73.7.4423-4426.2005
Source: PubMed

ABSTRACT

H2-M3-restricted CD8+ T cells can exhibit cross-reactivity to different bacterially derived N-formylmethionine peptides. The extent of this promiscuity is unclear. We deleted the nonredundant fMIVTLF epitope and found
that Listeria monocytogenes still primed fMIVTLF-specific T cells. Thus, cross-reactivity appears to be a more general characteristic of H2-M3-restricted
T cells.

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Available from: ncbi.nlm.nih.gov
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    • "It has been shown that some H2-M3–restricted LM-specific CTLs are cross-reactive with antigens derived from a variety of Gram-positive and Gram-negative bacteria (29). In addition, deletion of H2-M3–restricted epitopes from LM does not prevent the priming of H2-M3–restricted T cells with specificity for the deleted epitope, suggesting that promiscuous antigen recognition may be a feature common to many H2-M3–restricted T cells (30–32). The promiscuous recognition and cross-reactivity to common environmental bacteria may lead to the priming and expansion of LM-reactive H2-M3–restricted T cells in “naive” animals, resulting in increased precursor frequency as well as a “primed” state. "
    [Show abstract] [Hide abstract] ABSTRACT: 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.
    Full-text · Article · Mar 2006 · Journal of Experimental Medicine
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    [Show abstract] [Hide abstract] ABSTRACT: Not embargoed. Vita. Thesis (Ph.D.) -- University of Texas Southwestern Medical Center at Dallas, 2005. Bibliography: 114-132.
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    [Show abstract] [Hide abstract] ABSTRACT: 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 signifi cance of H2-M3-restricted T cells in host defense against bacteria is unclear. We generated H2-M3-defi cient mice to investigate the role of H2-M3 in immunity against Listeria monocytogenes (LM), a model intracellular bacterial pathogen. H2-M3-defi cient mice are impaired in early bacterial clearance during primary infection, with diminished LM-specifi c CD8+ T cell responses and compromised innate immune functions. Although H2-M3-restricted CD8+ T cells constitute a signifi cant 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-defi cient 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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