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PreprintCited by 2T-cell and B-cell ImmunologySignaling Pathways in DiseaseNF-κB Signaling Pathways

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ABIN1 is a negative regulator of effector functions in cytotoxic T cells

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Janusova, Sarka, Paprckova, Darina, Michalik, Juraj, Uleri, Valeria, Drobek, Ales, Salyova, Eva, Chorfi, Louise, Neuwirth, Ales, Prochazka, Jan, Sedlacek, Radislav, Draber, Peter, Stepanek, Ondrej·2023·EMBO Reports
DOI 10.1101/2023.10.25.563918PMC PMC11315980

Preprint — published as 10.1038/s44319-024-00179-6 · Paper page

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Abstract

T cells are pivotal in the adaptive immune defense, necessitating a delicate balance between robust response against infections and self-tolerance. Their activation involves intricate cross-talk among signaling pathways triggered by the T-cell antigen receptors (TCR) and co-stimulatory or inhibitory receptors. The molecular regulation of these complex signaling networks is still incompletely understood. We identified an adaptor protein, ABIN1 as a component of the signaling complexes of GITR and OX40 co-stimulation receptors. T cells lacking ABIN1 are hyper-responsive ex vivo, and exhibit enhanced responses to cognate infections, and superior ability to induce experimental autoimmune diabetes in mice. We observed that ABIN1 negatively regulates NF-κB and p38 pathways. The latter was at least partially responsible for the upregulation of key effector proteins, IFNG and GZMB in ABIN1-deficient T cells after TCR stimulation. Our findings reveal the intricate role of ABIN1 in T-cell regulation and its potential as a target for therapeutic fine-tuning of T-cell responses.

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Metadata

Authors
Janusova, S., Paprckova, D., Michalik, J., Uleri, V., Drobek, A., Salyova, E., Chorfi, L., Neuwirth, A., Prochazka, J., Sedlacek, R., Draber, P., & Stepanek, O.
Affiliations
Czech Academy of Sciences (CZ)
ORCID
Venue
EMBO Reports
Publisher
openRxiv
Published
2023-10-30
Volume
25
Issue
8
Pages
3456-3485
ISSN
1469-221X (ISSN-L)
DOI
10.1101/2023.10.25.563918
PMC
PMC11315980
OpenAlex
W4399677541
Cited by
2
References
1
Citations by year
2026: 1 · 2025: 1
FWCI
0.33
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • EMBO Reports (publishedVersion, cc-by)
  • bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by-nd)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • European Molecular Biology Organization (IG 4420)
  • Univerzita Karlova v Praze (CZ.1.05/1.1.00.02.0109, PRIMUS/20/MED/003, 68378050)
  • Grantová Agentura, Univerzita Karlova (274323, 984120, PRIMUS/20/MED/003)
  • Přírodovědecká Fakulta, Univerzita Karlova
  • European Commission (274323, LX22NPO5103, HORIZON2020, 802878, CZ.1.05/1.1.00/02.0109)
  • Ministerstvo Školství, Mládeže a Tělovýchovy (RVO-68378050-KAV-NPUI, LM2023050, OP RDI CZ.1.05/2.1.00/19.0395, LM2023036, OP RDI BIOCEV CZ.1.05/1.1.00/02.0109)
  • Grantová Agentura České Republiky (CZ.1.05/1.1.00/02.0109, RVO 68378050, 68378050, GA22-18046S)
  • Akademie Věd České Republiky (RVO68378050, 68378050‐KAV‐NPUI, OP RDI BIOCEV CZ.1.05/1.1.00/02.0109, BIOCEV CZ.1.05/1.1.00/02.0109, 68378050, LM2023036)
  • Ústav Molekulární Genetiky, Akademie Věd České Republiky (RVO:68378050, 68378050, 68378050-KAV-NPUI)
  • European Regional Development Fund (CZ.1.05/1.100/02.0109, BIOCEV CZ.1.05/1.1.00/02.0109.)
  • HORIZON EUROPE European Research Council (802878)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Keywords
cytotoxic T lymphocytes, T cell costimulation, GITR, OX40, p38 MAPK, NF-κB signaling, T cell effector function, interferon-gamma, granzyme B, experimental autoimmune diabetes, T cell tolerance, T cell receptor signaling
MeSH terms
Animals, Diabetes Mellitus, Type 1, Humans, Interferon-gamma, Lymphocyte Activation, Mice, Inbred C57BL, Receptors, Antigen, T-Cell, T-Lymphocytes, Cytotoxic, Signal Transduction, NF-kappa B, Mice, Knockout, p38 Mitogen-Activated Protein Kinases, Adaptor Proteins, Signal Transducing, Mice, Receptors, OX40, Glucocorticoid-Induced TNFR-Related Protein

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