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SOD-mimics are small complexes that reproduce the activity of superoxide dismutases, natural proteins that catalytically dismutate the superoxide anion. Activated macrophages, which produce ROS and RNS fluxes, constitute a relevant model to challenge antioxidant activity in a cellular context and were used to test a Mn-complex which was shown to efficiently alter the flow of O(2)(-), ONOO(-) and H(2)O(2).
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http://dx.doi.org/10.1039/c2dt12479c | DOI Listing |
Crit Rev Immunol
January 2025
Department of Biochemistry, University of Kerala, Kariavattom, Thiruvananthapuram, Kerala, India 695581.
Rheumatoid arthritis (RA) is a chronic autoimmune condition that impacts the immune system, especially through changes in the splenic immune cell system. This review provides an overview of the role of splenocytes in T cell signaling and their immune response in RA patients. The spleen acts as a critical site for the activation and differentiation of splenic immune cells like T cells, B cells, macrophages, dendritic cells, and NK cells.
View Article and Find Full Text PDFChem Biodivers
September 2025
College of Food Science and Technology, Shanghai Ocean University, Shanghai, China.
This research emphasized the extraction and separation of polysaccharides derived from Syzygium jambos (L.) Alston (PSJAP-5), as well as analyses of their structural characteristics and immunomodulatory activities. This study initially employed response surface methodology to determine the extraction conditions of polysaccharides.
View Article and Find Full Text PDFAm J Respir Cell Mol Biol
September 2025
Boston University School of Medicine, Department of Biochemistry & Cell Biology, Boston, Massachusetts, United States.
The increased presence of goblet epithelial cells in conducting airways of the respiratory system is common in pulmonary disorders and is often accompanied by disrupted immune and alveolar responses. Signaling effectors that restrict goblet cell production include YAP and TAZ, transcriptional regulators of Hippo signaling, which repress goblet cell differentiation in the airway epithelium. Here, we investigated the acute responses to goblet cell metaplasia that are induced by the conditional loss of YAP/TAZ in club epithelial cells of adult mouse lungs.
View Article and Find Full Text PDFPLoS Biol
September 2025
Department of Virology, Immunology & Microbiology, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, United States of America.
Despite the success of antiretroviral therapy in suppressing plasma viremia in people living with human immunodeficiency virus type-1 (HIV-1), persistent viral RNA expression in tissue reservoirs is observed and can contribute to HIV-1-induced immunopathology and comorbidities. Infection of long-lived innate immune cells, such as tissue-resident macrophages and microglia may contribute to persistent viral RNA production and chronic inflammation. We recently reported that de novo cytoplasmic expression of HIV-1 intron-containing RNA (icRNA) in macrophages and microglia leads to MDA5 and MAVS-dependent innate immune sensing and induction of type I IFN responses, demonstrating that HIV icRNA is a pathogen-associated molecular pattern (PAMP).
View Article and Find Full Text PDFPLoS Pathog
September 2025
Department of Virology, Immunology, and Microbiology, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, United States of America.
While human autopsy samples have provided insights into pulmonary immune mechanisms associated with severe viral respiratory diseases, the mechanisms that contribute to a clinically favorable resolution of viral respiratory infections remain unclear due to the lack of proper experimental systems. Using mice co-engrafted with a genetically matched human immune system and fetal lung xenograft (fLX), we mapped the immunological events defining successful resolution of SARS-CoV-2 infection in human lung tissues. Viral infection is rapidly cleared from fLX following a peak of viral replication, histopathological manifestations of lung disease and loss of AT2 program, as reported in human COVID-19 patients.
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