Kawasaki disease (KD) is an acute systemic vasculitis and activation of monocytes plays a central role in the pathogenesis of it. B10 cells, a B cell subset with negative regulatory properties, are functionally identified by their ability to express cytoplasmic IL-10 after ex vivo stimulation. Here, we aimed to explore the functional role of B10 cells during monocyte-mediated inflammatory responses in KD, as well as elucidate the underlying microRNA (miRNA)-mediated regulatory mechanisms. Expression of IL-10 by each group of B cells (total B cells, transitional B cells, naïve B cells, and memory B cells) and inhibition of monocyte-derived TNF-α by activated B cells were measured by flow cytometry. Expression of miRNAs (miR-21-3p, miR-98-5p/3p, miR-27a-3p, let7b-5p, and miR-1423p/5p) that affect IL-10 levels in B cells was quantitated by real-time PCR. The relationship between IL-10 and these miRNAs was examined by multivariate analysis. MiR-mediated RNA interference in B cells was performed to investigate the role of miR-27a on expression of IL-10. The results showed expression of cytoplasmic IL-10 in B cell subsets from patients with KD was down-regulated. The inhibitory effect of B10 cells on production of TNF-α by monocytes from patients with KD was also compromised. The miR-27a-3p expression was markedly up-regulated during the acute phrase of KD, and it promoted monocyte-mediated TNF-α release by negatively regulating expression of cytoplasmic IL-10 within B cells in vitro. The data suggest up-regulated miR-27a in B cells from patients with KD may promote monocyte-mediated inflammatory responses by inhibiting the regulatory function of B10 cells.
Introduction: Chronic alcohol consumption and tobacco usage are major risk factors for esophageal squamous cell carcinoma (ESCC). Excessive tobacco and alcohol consumption lead to oxidative stress and the generation of reactive carbonyl species (RCS) which induce DNA damage and cell apoptosis. This phenomenon contributes to cell damage and carcinogenesis in various organs including ESCC.
The pathobiont Staphylococcus aureus (Sa) induces nonprotective antibody imprints that underlie ineffective staphylococcal vaccination. However, the mechanism by which Sa modifies antibody activity is not clear. Herein, we demonstrate that IL-10 is the decisive factor that abrogates antibody protection in mice.
Metabolic rewiring is required for cancer cells to survive in harsh microenvironments and is considered to be a hallmark of cancer. Specific metabolic adaptations are required for a tumor to become invasive and metastatic. Cell division and metabolism are inherently interconnected, and several cell cycle modulators directly regulate metabolism.
Department of Gastrointestinal Surgery, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan 610072, P.R. China.
Cellular immunotherapy represents a pivotal treatment modality in clinical practice. Regulatory B cells (Bregs), a key subset of B lymphocytes, hold promise in the management of autoimmune diseases, cancer and transplantation immunity. The expansion of Bregs for cell therapy is a promising strategy to alleviate inflammation and promote immune tolerance.
Hippocampal area CA2 is unique in many ways, largely based on the complement of genes expressed there. We and others have observed that CA2 neurons exhibit a uniquely robust tropism for adeno-associated viruses (AAVs) of multiple serotypes and variants. In this study, we aimed to systematically investigate the propensity for AAV tropism toward CA2 across a wide range of AAV serotypes and variants, injected either intrahippocampally or systemically, including AAV1, 2, 5, 6, 8, 9, DJ, PHP.
