Publications by authors named "N Seta"
Role of Circulating Monocytes and Periodontopathic Bacteria in Pathophysiology of Rheumatoid Arthritis.
Bull Tokyo Dent Coll
December 2024
Article Synopsis
- Rheumatoid arthritis (RA) is driven by chronic inflammation in the synovial membrane, primarily caused by immune cells like macrophages and osteoclasts that lead to cartilage and bone destruction.
- Circulating monocytes differentiate into macrophages and osteoclasts in RA, with synovial macrophages categorized into proinflammatory (M1) and anti-inflammatory (M2) types.
- Recent studies highlight the link between various subsets of these immune cells and RA, along with a notable association between periodontopathic bacteria and the development of the disease.
Biologic drugs (therapeutic proteins or peptides) have become one of the most important therapeutic modalities over the past few decades. Drug-induced immunogenicity is a significant concern as it may affect safety, tolerability, and efficacy. With more sensitive and drug-tolerant screening assays in use today, reliable estimation of anti-drug-antibody (ADA) titer has become more important for understanding clinically relevant ADA levels.
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- SLC37A4 is a gene that codes for a protein essential for transporting glucose-6-phosphate into the endoplasmic reticulum, which is important for glucose metabolism, especially during times of glucose scarcity.
- Mutations in SLC37A4 lead to glycogen storage disorder 1b, which causes liver and kidney issues, along with a lack of certain white blood cells (neutropenia).
- Research on seven individuals with a specific mutation in SLC37A4 revealed liver dysfunction and abnormal serum glycans, and CRISPR technology was used to create liver cells mimicking the mutation's effects, connecting it to abnormal glycosylation and changes in cell structure.
Phosphoglucomutase 3 (PGM3) deficiency is a rare congenital disorder of glycosylation. Most of patients with autosomal recessive hypomorphic mutations in PGM3 encoding for phosphoglucomutase 3 present with eczema, skin and lung infections, elevated serum IgE, as well as neurological and skeletal features. A few PGM3-deficient patients suffer from a more severe disease with nearly absent T cells and severe skeletal dysplasia.
View Article and Find Full Text PDFSignal sequence receptor protein 4 (SSR4) is a subunit of the translocon-associated protein complex, which participates in the translocation of proteins across the endoplasmic reticulum membrane, enhancing the efficiency of N-linked glycosylation. Pathogenic variants in SSR4 cause a congenital disorder of glycosylation: SSR4-congenital disorders of glycosylation (CDG). We describe three SSR4-CDG boys and review the previously reported.
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