ArticleScientific reports2025
ITK overexpression enhances T cell cytotoxicity against DLBCL through the TCR-Ca
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
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4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Diffuse Large B-Cell Lymphoma (DLBCL) is the most prevalent pathological subtype of non-Hodgkin lymphoma (NHL). Patients with DLBCL often experience extremely poor prognoses due to drug resistance or relapse, and the limitations of existing treatment regimens are evident. This study focuses on the mechanistic role and clinical significance of interleukin-2-inducible T-cell kinase (ITK) in DLBCL. Through bioinformatics analysis, it was found that ITK, as a key molecule in the T Cell Receptor (TCR) signaling pathway, is significantly underexpressed in DLBCL. This underexpression is associated with a poorer overall survival (OS) of patients and exhibits a negative correlation with the expression of the immune checkpoint molecule Programmed Death Ligand 1 (PD-L1), suggesting its potential involvement in the regulation of T cell exhaustion. In vitro experiments demonstrated that overexpression of Itk significantly enhanced the immunological activity of mouse T lymphocytes (CTLL-2), activating the TCR-Ca
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