Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

T cell activation is critical for adaptive immunity, helping to protect the body from infection and tumors. A key step in this activation is signal transduction downstream of the T cell antigen receptor. This signaling involves several steps, with early ones occurring at the plasma membrane and others that occur later, after TCR internalization. The late steps in TCR signaling remain poorly understood. Since the TCR can signal after its internalization, we postulated that kinases abundantly expressed in T cells may regulate TCR signaling. This study focuses on two such enzymes: integrin-linked kinase (ILKs) and threonine-tyrosine kinase (TTKs), whose involvement in TCR signaling has not been previously studied. Using specific depletion of TTK and ILK by lentiviral shRNA, we show that in the absence of ILK and TTK, the early steps of TCR signaling are strongly enhanced, while IL-2 production by activated T cells is strongly decreased. These findings are relevant because TTK and ILK are both important targets in oncology, and our results show that their inhibition affects the activation of T cells, which play an essential role in anti-tumor defense.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12022052PMC
http://dx.doi.org/10.1038/s41598-025-99331-yDOI Listing

Publication Analysis

Top Keywords

tcr signaling
20
steps tcr
8
ttk ilk
8
tcr
7
signaling
6
integrin linked
4
kinase
4
linked kinase
4
kinase threonine
4
threonine tyrosine
4

Similar Publications

T-cell therapies have proven to be a promising treatment option for cancer patients in recent years, especially in the case of chimeric antigen receptor (CAR)-T cell therapy. However, the therapy is associated with insufficient activation of T cells or poor persistence in the patient's body, which leads to incomplete elimination of cancer cells, recurrence, and genotoxicity. By extracting the splice element of PD-1 pre-mRNA using biology based on CRISPR/dCas13 in this study, our ultimate goal is to overcome the above-mentioned challenges in the future.

View Article and Find Full Text PDF

Background: Although previous studies suggested associations between psoriasis and atopic dermatitis (AD), the directionality and causality of these relationships remain controversial. This study employed bidirectional Mendelian randomization to investigate the potential causal relationships between these two inflammatory skin conditions.

Methods: Genome-wide association statistics were obtained for psoriasis and AD from large-scale consortia and meta-analyses of genome-wide association studies.

View Article and Find Full Text PDF

The skin integrates diverse signals discerned by sensory neurons and immune cells to elicit adaptive responses to a range of stresses. Considering interactions between nervous and immune systems, we examined whether regulatory T (T) cells, which suppress systemic and local inflammation, can modulate activation of peripheral neurons. Acute T cell "loss of function" increased neuronal activation to noxious stimuli independently of their immunosuppressive function.

View Article and Find Full Text PDF

PTPN22-CD45 dual phosphatase retrograde feedback enhances TCR signaling and autoimmunity.

Sci Adv

September 2025

Department of Medicine, Altman Clinical and Translational Research Institute, University of California, San Diego, La Jolla, CA 92093, USA.

Protein tyrosine phosphatase nonreceptor type 22 (PTPN22) is encoded by a gene strongly associated with lupus and other autoimmune diseases. PTPN22 regulates T cell receptor (TCR) signaling through dephosphorylation of the kinases lymphocyte-specific protein tyrosine kinase (LCK) and zeta-chain-associated protein kinase 70 (ZAP70). The regulation of PTPN22 remains poorly understood.

View Article and Find Full Text PDF

Tumors frequently evade immune destruction by impairing cytotoxic CD8 T-cell responses, highlighting the need for strategies that restore T-cell functionality. Here, we identify SLAMF7 (CD319) as a key enhancer of human CD8 T-cell responses against tumors. SLAMF7 expression is induced by pro-inflammatory signals such as IL-12 and CD28 co-stimulation.

View Article and Find Full Text PDF