B-cell acute lymphoblastic leukemia (B-ALL) accounts for 85% of all childhood ALL. Malignancies exhaust T and B cells, resulting in an increased expression of immune checkpoint receptors (ICRs), such as T-cell immunoglobulin and mucin domain 3 (TIM-3). TIM-3 has been found to be dysregulated in different types of cancer. However, there is a lack of rigorous studies on the TIM-3 expression in B-ALL. The current study aimed to measure the expression of TIM-3 at the gene and protein levels and evaluate the potential of TIM-3 as a biomarker in B-ALL. A total of 28 subjects were recruited between 2021 and 2023, comprising 18 subjects diagnosed with B-ALL and 10 non-malignant healthy controls. The B-ALL patients were divided into three groups: newly diagnosed (four patients), in remission (nine patients), and relapse/refractory (five patients). The expression levels of TIM-3 were evaluated using the real-time qPCR and ELISA techniques. The results revealed that the TIM-3 expression was significantly downregulated in the malignant B-ALL patients compared to the non-malignant healthy controls in the mRNA (FC = -1.058 ± 0.3548, = 0.0061) and protein blood serum ( = 0.0498) levels. A significant TIM-3 gene reduction was observed in the relapse/refractory cases (FC = -1.355 ± 0.4686, = 0.0327). TIM-3 gene expression allowed for significant differentiation between patients with malignant B-ALL and non-malignant healthy controls, with an area under the curve (AUC) of 0.706. The current study addressed the potential of reduced levels of TIM-3 as a negative biomarker for B-ALL patients.
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http://dx.doi.org/10.3390/ijms252011148 | DOI Listing |
Clin Exp Rheumatol
December 2024
Faculty of Medicine, National Yang Ming Chiao Tung University, Taipei, and Division of Allergy, Immunology & Rheumatology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
Objectives: Deltex1 is a transcriptional target of NFAT that promotes T cell anergy. However, whether Deltex1 affects the properties of regulatory T cells (Tregs), which are involved in the pathogenesis of Sjögren's disease (SjD), is unknown.
Methods: T cells were purified from peripheral blood using a negative selection method.
Heliyon
November 2024
Research Institute for Internal Medicine, Oslo University Hospital, Oslo, Norway.
J Immunother Cancer
November 2024
Department of Surgery, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
Background: Gastric carcinomas (GC) are aggressive malignancies, and only ~15% of patients respond to anti-programmed cell death (ligand) 1 (PD-(L)1) monotherapy. However, Epstein-Barr virus (EBV)-associated GCs (~5-10% of GCs) often harbor PD-L1 and PD-L2 chromosomal amplifications and robust CD8+ T cell infiltrates, and respond at a high rate to anti-PD-1. The current study compares the tumor immune microenvironments (TiMEs) of EBV+ versus EBV(-) GCs.
View Article and Find Full Text PDFJ Neuroimmunol
January 2025
Department of Biomedical Sciences, Seoul National University Graduate School, Seoul, Republic of Korea; PB Immune Therapeutics Inc., Seoul, Republic of Korea; Transplantation Research Institute, Medical Research Center, Seoul National University, Seoul, Republic of Korea; Department of Microbiology and Immunology, College of Medicine, Seoul National University, Seoul, Republic of Korea; Cancer Research Institute, Seoul National University, Seoul, Republic of Korea; Genomic Medicine Institute, Medical Research Center, Seoul National University, Seoul, Republic of Korea. Electronic address:
Alzheimer's disease (AD) is a progressive neurological disorder and the leading cause of dementia. Despite significant efforts, treatment strategies targeting amyloid-β have been less successful than anticipated. Recently, the role of neuroinflammation and adaptive immune response in AD pathogenesis has gained attention.
View Article and Find Full Text PDFCells
October 2024
Fiona Elsey Cancer Research Institute, Ballarat, VIC 3350, Australia.
Inhibitory receptors are critical for regulating immune cell function. In cancer, these receptors are often over-expressed on the cell surface of T and NK cells, leading to reduced anti-tumor activity. Here, through the analysis of 11 commonly studied checkpoint and inhibitory receptors, we discern that only (TIM3) and (CD39) display significantly greater gene expression in glioblastoma compared to normal brain and lower grade glioma.
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