ArticleCell death & disease2018
IL-21 and anti-CD40 restore Bcl-2 family protein imbalance in vitro in low-survival CD27
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- B cells in cancer: functions, mechanisms and therapeutic advances.Signal transduction and targeted therapy · 2026Review
- CD40L and IL-4 lymph node-associated signals protect B cells from rituximab-induced ADCC via KIR and NKG2A.Clinical and experimental immunology · 2026Article
- Antibody Secretion Capacity in CVID Patients: Immunoglobulin Isotypes and Antigen Specificities After T-Cell-Dependent In Vitro Stimulation.Journal of clinical medicine · 2025Article
- Dysfunctional mitochondria, disrupted levels of reactive oxygen species, and autophagy in B cells from common variable immunodeficiency patients.Frontiers in immunology · 2024Article
- Decreased ATM Function Causes Delayed DNA Repair and Apoptosis in Common Variable Immunodeficiency Disorders.Journal of clinical immunology · 2021Article
- Defective Bcl-2 expression in memory B cells from common variable immunodeficiency patients.Clinical and experimental immunology · 2021Article
- Connection of BANK1, Tolerance, Regulatory B cells, and Apoptosis: Perspectives of a Reductionist Investigation.Frontiers in immunology · 2021Article
- Primary Humoral Immune Deficiencies: Overlooked Mimickers of Chronic Immune-Mediated Gastrointestinal Diseases in Adults.International journal of molecular sciences · 2020Review
- Functions of Tfh Cells in Common Variable Immunodeficiency.Frontiers in immunology · 2020Review
- Partial Protection From Lupus-Like Disease by B-Cell Specific Type I Interferon Receptor Deficiency.Frontiers in immunology · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Common variable immunodeficiency (CVID) is characterized by an abnormal B cell differentiation to memory and antibody-secreting B cells. The defective functionality of CVID patients' B cells could be the consequence of alterations in apoptosis regulation. We studied the balance of Bcl-2 family anti-/pro-apoptotic proteins to identify molecular mechanisms that could underlie B cell survival defects in CVID. We used flow cytometry to investigate Bcl-2, Bcl-XL, Bax, and Bim expression in B cells ex vivo and after anti-CD40 or anti-BCR activation with or without IL-21, besides to spontaneous and stimulation-induced Caspase-3 activation and viable/apoptotic B cell subpopulations. We found increased basal levels of Bax and Bim in CVID B cells that correlated with low viability and high Caspase-3 activation only in CD27
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.