ArticleFrontiers in immunology2024
Dysfunctional mitochondria, disrupted levels of reactive oxygen species, and autophagy in B cells from common variable immunodeficiency patients.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Are Selenium Status and Inflammation Linked to Cardiometabolic Risk Factors in Inborn Errors of Immunity?Nutrients · 2026Article
- Altered duodenal N6-methyladenosine levels in common variable immunodeficiency associate with duodenal microbiota.Frontiers in immunology · 2026Article
- Intravenous immunoglobulin remodels innate immune cell communication and induces differential autophagy pathways in Kawasaki disease.Frontiers in immunology · 2026Article
- Integrated bioinformatics analysis unravels mitochondrial-immune crosstalk and infiltration dynamics in sepsis progression.European journal of medical research · 2025Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Common Variable Immunodeficiency (CVID) patients are characterized by hypogammaglobulinemia and poor response to vaccination due to deficient generation of memory and antibody-secreting B cells. B lymphocytes are essential for the development of humoral immune responses, and mitochondrial function, hreactive oxygen species (ROS) production and autophagy are crucial for determining B-cell fate. However, the role of those basic cell functions in the differentiation of human B cells remains poorly investigated. Methods: We used flow cytometry to evaluate mitochondrial function, ROS production and autophagy processes in human naïve and memory B-cell subpopulations in unstimulated and stimulated PBMCs cultures. We aimed to determine whether any alterations in these processes could impact B-cell fate and contribute to the lack of B-cell differentiation observed in CVID patients. Results: We described that naïve CD19 Conclusion: The failure in ROS cell signalling could impair CVID naïve B cell activation and differentiation to memory B cells. Decreased levels of ROS in CVID memory CD19
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