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Tumor-necrosis factor α-rich environment alters type-I interferon response to viral stimuli in patients with juvenile idiopathic arthritis by altering myeloid dendritic cell phenotype

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00064203%3A_____%2F24%3A10478338" target="_blank" >RIV/00064203:_____/24:10478338 - isvavai.cz</a>

  • Alternative codes found

    RIV/00216208:11130/24:10478338

  • Result on the web

    <a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=Q-fa9F7NTI" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=Q-fa9F7NTI</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1016/j.clim.2024.110170" target="_blank" >10.1016/j.clim.2024.110170</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Tumor-necrosis factor α-rich environment alters type-I interferon response to viral stimuli in patients with juvenile idiopathic arthritis by altering myeloid dendritic cell phenotype

  • Original language description

    The balance between the tumor-necrosis factor α (TNFα) and type-I interferon (T1IFN) pathways is crucial for proper immune function. Dysregulation of either pathway can contribute to autoimmune diseases development. Even though TNFα blockade has shown promising results in various autoimmune diseases, the effect on the balance between TNFα and T1IFN is elusive. We used targeted anti-TNFα therapies in juvenile idiopathic arthritis (JIA) as an experimental approach to study the cross-regulation between TNFα and type-I IFN. We found that TNFα-rich environment affected viral defense through the attenuation of T1IFN responses and affected the phenotype and distribution of myeloid dendritic cells, which are engaged in early viral infections. Anti-TNFα therapy normalized the observed deviations in JIA patients. We hypothesize that the inadequate immune response caused by a high TNFα environment could be projected to more frequent or lengthy viral infections and possibly play a role in the process of JIA disease development.

  • 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

    30102 - Immunology

Result continuities

  • Project

    <a href="/en/project/NU20-05-00320" target="_blank" >NU20-05-00320: Neutrophils in juvenile idiopathic arthritis: biomarkers with potential to improve clinical treatment decisions and patient care</a><br>

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Others

  • Publication year

    2024

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Clinical Immunology

  • ISSN

    1521-6616

  • e-ISSN

    1521-7035

  • Volume of the periodical

    262

  • Issue of the periodical within the volume

    May

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    12

  • Pages from-to

    110170

  • UT code for WoS article

    001209250900001

  • EID of the result in the Scopus database

    2-s2.0-85187514049