We describe a sequence of reciprocal interactions between cloned inducer T cells and antigen-presenting cells (APC) that results in selective depletion of the antigen-reactive inducer cells. We show that corecognition of antigen and I-A by hapten-reactive inducer T cell clones results in (a) release of macrophage-activating factor (MAF) and other lymphokines, (b) expression of lytic activity by a subset of MAF-sensitized APC after triggering, and (3) lysis (mediated by the activated and triggered macrophage) of the inducer T cell clone and other cells in the vicinity. We suggest that this sequence of steps may limit the extent of macrophage-mediated tissue destruction by depleting the specific inducer T cell clones that initiate the response.
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http://dx.doi.org/10.1084/jem.158.4.1243 | DOI Listing |
World J Oncol
February 2025
Department of Surgical Oncology, Roswell Park Comprehensive Cancer Center, Buffalo, NY 14203, USA.
Background: Vascular endothelial growth factor-A (VEGFA) is a key inducer of angiogenesis, responsible for generating new blood vessels in the tumor microenvironment (TME) and facilitating metastasis. Notably, Avastin, which targets VEGFA, failed to demonstrate any significant benefit in clinical trials for breast cancer (BC). This study aimed to investigate the clinical relevance of gene expression in BC.
View Article and Find Full Text PDFImmunohorizons
January 2025
Department of Medical Microbiology and Infection Prevention, Amsterdam UMC location University of Amsterdam, Amsterdam, the Netherlands.
Atopic dermatitis (AD) is characterized by dysregulated T cell immunity and skin microbiome dysbiosis with predominance of Staphylococcus aureus, which is associated with exacerbating AD skin inflammation. Specific glycosylation patterns of S. aureus cell wall structures amplify skin inflammation through interaction with Langerhans cells (LCs).
View Article and Find Full Text PDFFree Radic Biol Med
January 2025
Institute of Systems Biomedicine, School of Basic Medical Sciences, Department of Pathology, Beijing Key Laboratory of Tumor Systems Biology, Peking University Health Science Center, Beijing 100191, China. Electronic address:
Cuproptosis, a copper-dependent form of regulated cell death, has been implicated in the progression and treatment of various tumors. The copper ionophores, such as Disulfiram (DSF), an FDA-approved drug previously used to treat alcohol dependence, have been found to induce cuproptosis. However, the limited solubility and effectiveness of the combination of DSF and copper ion restrict its widespread application.
View Article and Find Full Text PDFDokl Biochem Biophys
January 2025
National Research University Higher School of Economics, Moscow, Russia.
Ferroptosis is an iron-dependent form of programmed cell death (PCD) associated with lipid membrane peroxidation. It has gained attention in cancer research because some tumor cells that are resistant to other forms of PCD are sensitive to ferroptosis. Despite the significant amount of research on ferroptosis, the list of known inducers remains limited, creating opportunities to discover new compounds with clinical potential.
View Article and Find Full Text PDFImmunohorizons
January 2025
Center for Translational Immunology, Benaroya Research Institute at Virginia Mason, Seattle, WA, United States.
Dysregulated differentiation of naïve CD4+ T cells into T helper 17 (Th17) cells is likely a key factor predisposing to many autoimmune diseases. Therefore, better understanding how Th17 differentiation is regulated is essential to identify novel therapeutic targets and strategies to identify individuals at high risk of developing autoimmunity. Here, we extend our prior work using chemical inhibitors to provide mechanistic insight into a novel regulator of Th17 differentiation, the kinase dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A).
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