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Substrate-specific presentation of MHC class I-restricted antigens via autophagy pathway

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00209805%3A_____%2F22%3A00079008" target="_blank" >RIV/00209805:_____/22:00079008 - isvavai.cz</a>

  • Result on the web

    <a href="https://www.sciencedirect.com/science/article/abs/pii/S0008874922000089?via%3Dihub" target="_blank" >https://www.sciencedirect.com/science/article/abs/pii/S0008874922000089?via%3Dihub</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1016/j.cellimm.2022.104484" target="_blank" >10.1016/j.cellimm.2022.104484</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Substrate-specific presentation of MHC class I-restricted antigens via autophagy pathway

  • Original language description

    The accumulation of protein aggregates is toxic and linked to different diseases such as neurodegenerative disorders, but the role of the immune system to target and destroy aggregate-carrying cells is still relatively unknown. Here we show a substrate-specific presentation of antigenic peptides to the direct MHC class I pathway via autophagy. We observed no difference in presentation of peptides derived from the viral EBNA1 protein following suppression of autophagy by knocking down Atg5 and Atg12. However, the same knock down treatment suppressed the presentation from ovalbumin. Fusing the aggregate-prone poly-glutamine (PolyQ) to the ovalbumin had no effect on antigen presentation via autophagy. Interestingly, fusing the EBNA1-derived gly-ala repeat (GAr) sequence to ovalbumin rendered the presentation Atg5/12 independent. We also demonstrate that the relative levels of protein expression did not affect autophagy-mediated antigen presentation. These data suggest a substrate-dependent presentation of antigenic peptides for the MHC class I pathway via autophagy and indicate that the GAr of the EBNA1 illustrates a novel virus-mediated mechanism for immune evasion of autophagy-dependent antigen presentation.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    10608 - Biochemistry and molecular biology

Result continuities

  • Project

    <a href="/en/project/EF16_019%2F0000868" target="_blank" >EF16_019/0000868: Molecular, cellular and clinical approach to healthy ageing</a><br>

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2022

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    CELLULAR IMMUNOLOGY

  • ISSN

    0008-8749

  • e-ISSN

    1090-2163

  • Volume of the periodical

    374

  • Issue of the periodical within the volume

    April 2022

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    10

  • Pages from-to

    104484

  • UT code for WoS article

    000804064100005

  • EID of the result in the Scopus database

    2-s2.0-85125541048