| First Author | Janusova S | Year | 2024 |
| Journal | EMBO Rep | Volume | 25 |
| Issue | 8 | Pages | 3456-3485 |
| PubMed ID | 38877170 | Mgi Jnum | J:353049 |
| Mgi Id | MGI:7707533 | Doi | 10.1038/s44319-024-00179-6 |
| Citation | Janusova S, et al. (2024) ABIN1 is a negative regulator of effector functions in cytotoxic T cells. EMBO Rep |
| abstractText | 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-kappaB 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. |
