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Oral mucositis (OM) is a significant complication of cancer therapy with limited management strategies. Whilst inflammation is a central feature of destructive and ultimately ulcerative pathology, to date, attempts to mitigate damage via this mechanism have proven limited. A relatively underexamined aspect of OM development is the contribution of elements of the innate immune system. In particular, the role played by barriers, pattern recognition systems, and microbial composition in early damage signaling requires further investigation. As such, this review highlights the innate immune response as a potential focus for research to better understand OM pathogenesis and development of interventions for patients treated with radiotherapy and chemotherapy. Future areas of evaluation include manipulation of microbial-mucosal interactions to alter cytotoxic sensitivity, use of germ-free models, and translation of innate immune-targeted agents interrogated for mucosal injury in other regions of the alimentary canal into OM-based clinical trials.
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http://dx.doi.org/10.3390/ijms242216314 | DOI Listing |
Proc Natl Acad Sci U S A
September 2025
Centre for Experimental Medicine & Rheumatology, William Harvey Research Institute and Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, United Kingdom.
MS4A4A belongs to the MS4A tetraspan protein superfamily and is selectively expressed by the monocyte-macrophage lineage. In this study, we aimed to evaluate the role of MS4A4A+ macrophages in rheumatoid arthritis (RA) pathogenesis and response to treatment. RNA sequencing and immunohistochemistry of synovial samples from either early treatment-naïve or active chronic RA patients showed that MS4A4A expression positively correlated with synovial inflammation.
View Article and Find Full Text PDFInfect Immun
September 2025
Institute of Medical Microbiology and Hospital Hygiene, Heinrich Heine University, Düsseldorf, Germany.
Lymphotoxin β receptor (LTβR/TNFRSF3) signaling plays a crucial role in immune defense. Notably, LTβR-deficient (LTβR) mice exhibit severe defects in innate and adaptive immunity against various pathogens and succumb to infection. Here, we investigated the bone marrow (BM) and peritoneal cavity (PerC) compartments of LTβR mice during infection, demonstrating perturbed B-cell and T-cell subpopulations in the absence of LTβR signaling.
View Article and Find Full Text PDFInfect Immun
September 2025
School of Veterinary Medicine and Biomedical Sciences, University of Nebraska, Lincoln, Nebraska, USA.
Cell death mechanisms play a fundamental role in mycobacterial pathogenesis. We critically reviewed 94 research manuscripts, 44 review articles, and 4 book chapters to analyze important discoveries, background literature, and potential shortcomings in the field. The focus of this review is the pathogen (Mtb) and other Mtb and complex microorganisms.
View Article and Find Full Text PDFCell Biochem Biophys
September 2025
Department of Molecular Biology and Genetics, Faculty of Engineering and Natural Sciences, Istinye University, Istanbul, 34003, Türkiye, Turkey.
Vitamin B12 is a vital water-soluble vitamin containing a central cobalt atom within its corrin ring structure. It exists in several derivatives, among which methylcobalamin (MeCbl) and adenosylcobalamin (AdCbl) are the biologically active forms that serve as cofactors in essential enzymatic reactions. Although the neurological and hematological consequences of vitamin B12 deficiency have been extensively studied, its role in immune regulation remains less well understood.
View Article and Find Full Text PDFRheumatol Int
September 2025
Clinical Department of Rheumatology, Immunology and Internal Medicine, University Hospital in Kraków, Jakubowskiego 2, Kraków, 30-688, Poland.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by complex disturbances in both innate and adaptive immune responses, often leading to multi-organ involvement. One of the key features of SLE pathogenesis is endothelial dysfunction, which contributes to immune cell infiltration and vascular inflammation. In this context, adhesion molecules such as platelet endothelial cell adhesion molecule-1 (PECAM-1), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) may reflect the degree of endothelial activation.
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