() persists as latent infection in nearly a quarter of the global population and remains the leading cause of death among infectious diseases. While BCG is the only vaccine for TB, its inability to provide complete protection makes it imperative to engineer BCG such that it expresses immunodominant antigens that can enhance its protective potential. comparative genomic analysis of Mycobacterium species identified Rv1507A as a "signature protein" found exclusively in . (cell lines) and experiments carried out in mice, using purified recombinant Rv1507A revealed it to be a pro-inflammatory molecule, eliciting significantly high levels of IL-6, TNF-α, and IL-12. There was increased expression of activation markers CD69, CD80, CD86, antigen presentation molecules (MHC I/MHCII), and associated Th1 type of immune response. Rv1507A knocked-in also induced significantly higher pro-inflammatory Th1 response and higher survivability under stress conditions, both (macrophage RAW264.7 cells) and (mice). Sera derived from human TB patients showed significantly enhanced B-cell response against Rv1507A. The ability of Rv1507A to induce immuno-modulatory effect, B cell response, and significant memory response, renders it a putative vaccine candidate that demands further exploration.
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http://dx.doi.org/10.3389/fimmu.2020.01199 | DOI Listing |
Clin Epigenetics
January 2025
Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Background: The primary objective of this study was to examine whether ARID1A mutations confer a fitness advantage to gastric cancer from an immunological perspective, along with elucidating the underlying mechanism. Additionally, we aimed to identify the clinical potential of combining epigenetic inhibitors with immune checkpoint inhibitors to improve the efficacy of immunotherapy for gastric cancer.
Methods: The correlation between ARID1A gene expression and gastric cancer patient survival was analyzed using the GEO dataset GSE62254.
Ecotoxicol Environ Saf
January 2025
NHC Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, Jilin 130021, PR China. Electronic address:
Exposure of PM2.5 can cause different degrees of lung injury, which is referred with inflammatory response. Some evidences showed that low-dose radiation (LDR) induces hormesis in immune, however, it is unknown if LDR ameliorates the PM2.
View Article and Find Full Text PDFClin Rev Allergy Immunol
December 2024
Division of Allergy and Clinical Immunology, The Johns Hopkins Asthma & Allergy Center, Johns Hopkins University School of Medicine, 5501 Hopkins Bayview Circle, Room 3B.71, Baltimore, MD, 21224, USA.
Asthma is a chronic airway inflammatory disease that affects millions globally. Although glucocorticoids are a mainstay of asthma treatment, a subset of patients show resistance to these therapies, resulting in poor disease control and increased morbidity. The complex mechanisms underlying steroid-resistant asthma (SRA) involve Th1 and Th17 lymphocyte activity, neutrophil recruitment, and NLRP3 inflammasome activation.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Gastroenterology, Fifth Affiliated Hospital, Zhengzhou University, Zhengzhou, China.
The deregulation of immune responses is what causes food allergy (FA) to occur. FA's cause is still unknown. The goal of this study is to investigate the mechanism how the impaired production of IL-10 occurs in peripheral naive B cells of patients with FA.
View Article and Find Full Text PDFChemosphere
January 2025
Laboratoire Chrono-Environnement, UMR 6249, CNRS/Université de Franche-Comté, 16 route de Gray, 25000, Besançon, France.
For decades, studies have shown how exposure to non-essential trace metals such as lead (Pb) and cadmium (Cd) largely impact global wildlife. Ecoimmunotoxicology has emerged in the past two decades and focuses on the effects of pollutants on the immune system of free-ranging organisms. Adverse outcome pathways (AOPs) represent a conceptual approach to explore the mechanistic linkage between a molecular initiating event and adverse outcomes, potentially at all biological levels of organisation.
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