ABIN1 is a negative regulator of effector functions in cytotoxic T cells
Open accessPublished version of a preprint
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. Here, we identify the 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, exhibit enhanced responses to cognate infections, and superior ability to induce experimental autoimmune diabetes in mice. ABIN1 negatively regulates p38 kinase activation and late NF-κB target genes. P38 is at least partially responsible for the upregulation of the 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.
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Cites
Subramanian, A., Tamayo, P., Mootha, V. K., Mukherjee, S., Ebert, B. L., Gillette, M. A., Paulovich, A., Pomeroy, S. L., Golub, T. R., Lander, E. S., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0506580102 · Cited by 53,625 · see citing works
Global quantification of mammalian gene expression control
Schwanhäusser, B., Busse, D., Li, N., Dittmar, G., Schuchhardt, J., Wolf, J., Chen, W., & Selbach, M. (2011) · Nature · doi:10.1038/nature10098 · Cited by 6,566 · cited 1× · see citing works
“Label-free quanti fi cation was performed using the Intensity Based Absolute Quanti fi cation (iBAQ) algorithm, which divides the sum of all precursor-peptide intensities by the number of theoretically observable peptides (Schwanhäusser et al, 2011).”
LUBAC-mediated linear ubiquitination: a crucial regulator of immune signaling
IWAI, K. (2021) · Proceedings of the Japan Academy, Series B · doi:10.2183/pjab.97.007 · Cited by 37 · see citing works
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- Authors
- Janusova, S., Paprckova, D., Michalik, J., Uleri, V., Drobek, A., Salyova, E., Chorfi, L., Neuwirth, A., Andreyeva, A., Prochazka, J., Sedlacek, R., Draber, P., & Stepanek, O.
- Affiliations
- Czech Academy of Sciences (CZ)
- ORCID
- Venue
- EMBO Reports
- Published
- 2024-06-14
- Volume
- 25
- Issue
- 8
- Pages
- 3456-3485
- ISSN
- 1469-221X (ISSN-L)
- 1469-3178
- PMC
- PMC11315980
- OpenAlex
- W4399677541
- Cited by
- 2
- References
- 3
- Citations by year
- 2026: 1 · 2025: 1
- FWCI
- 0.33
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- 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
- Grantová Agentura České Republiky (22-18046S)
- European Union - Next Generation EU (LX22NPO5103)
- European Molecular Biology Organization (IG 4420)
- Univerzita Karlova v Praze (PRIMUS/20/MED/003)
- Grantová Agentura, Univerzita Karlova (984120, 274323)
- EC | ERC | HORIZON EUROPE European Research Council (802878)
- Ministerstvo Školství, Mládeže a Tělovýchovy (OP RDI CZ.1.05/2.1.00/19.0395, LM2023036, OP RDI BIOCEV CZ.1.05/1.1.00/02.0109, LM2023050, RVO - 68378050-KAV-NPUI)
- Ústav molekulární genetiky, AVČR core funding (RVO 68378050)
- 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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