Publications by authors named "C F Degos"
Article Synopsis
- TNFRSF14/HVEM is linked to immune response regulation and tumor progression, with its overexpression correlating to poorer prognosis in cancer patients.
- Researchers developed mouse models that mimic human BTLA and HVEM interactions to study the effects of a specific antibody (anti-HVEM18-10) on T cell activity in cancer environments.
- The findings indicate that anti-HVEM18-10 enhances T cell responses against tumors, decreases the presence of exhausted T cells, and leads to lasting tumor immunity, suggesting its potential as a therapeutic option in cancer treatment.
The strategies by which intracellular pathogenic bacteria manipulate innate immunity to establish chronicity are poorly understood. Here, we show that Brucella abortus outer membrane protein Omp25 specifically binds the immune cell receptor SLAMF1 in vitro. The Omp25-dependent engagement of SLAMF1 by B.
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- Endometrial cancer is the most prevalent cancer in the female genital tract in developed countries, with rising incidence linked to aging and obesity, making it a public health concern.
- The immune environment of endometrial cancer, particularly the role of NK cells, has not been extensively studied compared to other cancers.
- Findings indicate that NK cells are depleted in the tumor, showing increased expression of inhibitory molecules and reduced cytotoxicity due to altered chemokine and cytokine profiles in the tumor microenvironment, which fosters tumor growth.
Brucella is a Gram-negative bacterium responsible for brucellosis, a worldwide re-emerging zoonosis. Brucella has been shown to infect and replicate within Granulocyte macrophage colony-stimulating factor (GMCSF) in vitro grown bone marrow-derived dendritic cells (BMDC). In this cell model, Brucella can efficiently control BMDC maturation.
View Article and Find Full Text PDFThe detection of the activities of pathogen-encoded virulence factors by the innate immune system has emerged as a new paradigm of pathogen recognition. Much remains to be determined with regard to the molecular and cellular components contributing to this defense mechanism in mammals and importance during infection. Here, we reveal the central role of the IL-1β signaling axis and Gr1+ cells in controlling the Escherichia coli burden in the blood in response to the sensing of the Rho GTPase-activating toxin CNF1.
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