In recent years, conclusive data have emerged on a relationship between immune system, especially the T-cell, and blood pressure (BP). The objective of the present study was to determine the association between BP and four polymorphisms in CD80, CD86, CD28 and CTLA4 genes that code for key proteins in the T-cell co-stimulation process, in a female cohort. To that end, an association study in a cohort of 934 women over 40 years old from two hospitals was done. Raw data showed a significant association between the SNP rs1129055 of CD86 gene and BP. Analyzing this association against inheritance patterns, higher SBP (p < 0.000) and DBP (p = 0.005) values were observed in AA than in GG/GA genotype subjects in the largest sample cohort (Hospital 1). In multivariate linear regression studies, with adjustment for presumed independent predictors of BP, the SNP of the CD86 gene remained a predictor of SBP (p = 0.001) and DBP (p = 0.006), as did the SNP rs867234 of the CD80 gene for DBP (p < 0.000), both resisting the Bonferroni correction for multiple comparisons. As conclusion, we report a robust association between the SNP rs1129055 of CD86 gene and BP. The SNP rs867234 of CD80 gene was also shown to be a strong predictor of DBP.
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http://dx.doi.org/10.1016/j.gene.2020.144838 | DOI Listing |
J Leukoc Biol
December 2024
Department of Microbiology, Biochemistry and Molecular Genetics, Center for Cell Signaling, Rutgers New Jersey Medical School, 205 South Orange Ave, Newark, NJ, 07103.
While widely viewed as inhibitory receptors that drive efferocytosis and immune resolution on myeloid cells, TAM family members, particularly Mertk, have emerged as promising targets in immune-oncology to help stimulate host anti-tumor immunity. A recent study shows that Mertk expressed on human T cells, including CD8+ T cells and differentiated central memory T cells, has a co-stimulatory function for the T Cell Receptor (TCR). These new findings reveal the complexity and diversification of Mertk in immune regulation and its implications to cancer therapeutics.
View Article and Find Full Text PDFNat Cancer
December 2024
Genentech, South San Francisco, CA, USA.
Blockade of immune checkpoints PD-1 and TIGIT has demonstrated activity in mouse tumor models and human patients with cancer. Although these coinhibitory receptors can restrict signaling in CD8 T cells by regulating their associated co-stimulatory receptors CD28 and CD226, the functional consequences of combining PD-1 and TIGIT blockade remain poorly characterized. In mouse tumor models, we show that combination blockade elicited CD226-driven clonal expansion of tumor antigen-specific CD8 T cells.
View Article and Find Full Text PDFBreast Cancer Res Treat
December 2024
Department of Pathology, The Fourth Hospital of Hebei Medical University, No. 12 Jiankang Road, Shijiazhuang, 050011, Hebei, China.
Background: This study aimed to explore the correlation between primary tumors (PT) and paired metastatic lymph nodes (LN) and to develop a predictive model to provide evidence for forecasting patient prognoses.
Methods: We obtained single-cell and bulk transcriptome data from the Gene Expression Omnibus database. Furthermore, mRNA transcriptomic data, encompassing 112 normal tissues and 1066 breast cancer samples, along with survival, clinical, and mutation information for breast cancer patients, were acquired from The Cancer Genome Atlas (TCGA).
Diabetologia
December 2024
Diabetes Institute, College of Medicine, University of Florida, Gainesville, FL, USA.
Aims/hypothesis: Immunotherapeutics targeting T cells are crucial for inhibiting autoimmune disease progression proximal to disease onset in type 1 diabetes. There is an outstanding need to augment the durability and effectiveness of T cell targeting therapies by directly restraining proinflammatory T cell subsets, while simultaneously augmenting regulatory T cell (Treg) activity. Here, we present a novel strategy for preventing diabetes incidence in the NOD mouse model using a blocking monoclonal antibody targeting the type 1 diabetes risk-associated T cell co-stimulatory receptor, CD226.
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