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Differential capacity of T cell priming in naive donors of promiscuous CD4+ T cell epitopes of HCV NS3 and Core proteins.

Differential capacity of T cell priming in naive donors of promiscuous CD4+ T cell epitopes of HCV NS3 and Core proteins. Research Abstract Details 

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  • Differential capacity of T cell priming in naive donors of promiscuous CD4+ T cell epitopes of HCV NS3 and Core proteins. Abstract Text:

    florence a castelliFlorence A Castelli, leleu Leleu,sandra pouvelle-moratilleSandra Pouvelle-Moratille,sandrine farciSandrine Farci,hassane m zarourHassane M Zarour,muriel andrieuMuriel Andrieu,claude auriaultClaude Auriault, ,bertrand georgesBertrand Georges,bernard maillereBernard Maillere,

    To understand the inter-individual and virus-independent variability of CD4+ T cell responses to HCV components, we evaluated the effect on these responses of HLA II molecules in uninfected healthy donors. Using HLA II-specific binding assays, we identified, in the Core and NS3 proteins, 21 long fragments and 24 15-mer peptides that bound to four to eight of the most preponderant HLA II molecules. We then evaluated the priming capacity of eight long promiscuous peptides in 12 HLA-unrelated healthy donors. The NS3 1250-1264 peptide primed T cells in all the naive donors, while five others were stimulating in at least half of the individuals. We also report sequences that bind to multiple HLA II molecules but are weakly immunogenic. We therefore conclude that (i) broad HLA II specificity is only a prerequisite for a peptide to be stimulating in multiple individuals, and (ii) promiscuous peptides widely differ in their capacity to prime CD4+ T cells from uninfected healthy donors. We suggest that these priming differences result from inter-individual variations in the peptide-specific T cell repertoire. Interestingly, five of the most immunogenic peptides we identified correspond to frequently targeted T cell epitopes in infected patients.

    Differential capacity of T cell priming in naive donors of promiscuous CD4+ T cell epitopes of HCV NS3 and Core proteins. Publishing Authors By Initials

    fa castelliFA Castelli,m leleuM Leleu,s pouvelle-moratilleS Pouvelle-Moratille,s farciS Farci,hm zarourHM Zarour,m andrieuM Andrieu,c auriaultC Auriault,a A ,b georgesB Georges,b maillereB Maillere,

    For similar proteins: viral proteins: viral nonstructural proteins research abstracts see: proteins: viral proteins: viral nonstructural proteins research

    PUBMED ID PMID:

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    Differential capacity of T cell priming in naive donors of promiscuous CD4+ T cell epitopes of HCV NS3 and Core proteins. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: European journal of immunology

    VOLUME: 37

    Page Numbers: 1513-23

    Journal Abbreviation: Eur. J. Immunol.

    ISSN: 0014-2980

    DAY: 3

    MONTH: Jun

    YEAR: 2007

    Differential capacity of T cell priming in naive donors of promiscuous CD4+ T cell epitopes of HCV NS3 and Core proteins. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 1273201

    Differential capacity of T cell priming in naive donors of promiscuous CD4+ T cell epitopes of HCV NS3 and Core proteins. Keywords Mesh Terms:

    KEYWORDS: Viral Nonstructural Proteins

    MESH TERMS: immunology

    Chemical & Substance for Abstract: Differential capacity of T cell priming in naive donors of promiscuous CD4+ T cell epitopes of HCV NS3 and Core proteins. Information

    Substance Name: Interferon Type II

    Registry Number: 82115-62-6

    Grant and Affiliation Information for Differential capacity of T cell priming in naive donors of promiscuous CD4+ T cell epitopes of HCV NS3 and Core proteins.

    AFFILIATION: CEA, iBiTecS, Service d'Ingénierie Moléculaire des Protéines, Gif Sur Yvette, France.

    Country: Germany

    Germany Research PublicationGermany Research Publication

    AGENCY: United States NCI

    GRANT: CA90360

    ACRONYM: CA

    MEDLINETA: Eur J Immunol

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

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