ReviewFrontiers in immunology2017
Epstein-Barr Virus Susceptibility in Activated PI3Kδ Syndrome (APDS) Immunodeficiency.
Review in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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Who cites it
30 citing papers in PubMed, 46 citations in OpenAlex.
- Trial
- Lymphoproliferation in inborn errors of immunity: From challenging diagnosis to histologic revision.Journal of human immunity · 2026Article
- Case Report: Recurrent pulmonary infections with neck masses: a diagnostic challenge and literature review.Frontiers in medicine · 2026Article
- Interpreting the role of epigallocatechin-3-gallate in Epstein-Barr virus infection-mediated neuronal diseases.Folia microbiologica · 2025Article
- Overall survival among patients with activated phosphoinositide 3-kinase delta syndrome (APDS).Orphanet journal of rare diseases · 2025Article
- Gastric carcinoma harbouring loss‑of‑function mutations in theOncology letters · 2025Article
- Report of the Italian Cohort with Activated Phosphoinositide 3-Kinase δ Syndrome in the Target Therapy Era.Journal of clinical immunology · 2024Article
- Activated phosphoinositide 3-kinase delta syndrome: Pathogenesis, clinical manifestations, and treatment.Pediatric discovery · 2024Review
- Activated phosphoinositde 3-kinase (PI3Kδ) syndrome: an Italian point of view on diagnosis and new advances in treatment.Italian journal of pediatrics · 2024Review
- [Activated phosphoinositide 3-kinase delta syndrome: report of seven cases].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024Article
- Piloting an automated query and scoring system to facilitate APDS patient identification from health systems.Frontiers in immunology · 2024Article
- PI3Kδ Pathway Dysregulation and Unique Features of Its Inhibition by Leniolisib in Activated PI3Kδ Syndrome and Beyond.The journal of allergy and clinical immunology. In practice · 2024Article
- Case Report: Early-onset or recalcitrant cytopenias as presenting manifestations of activated PI3Kδ syndrome.Frontiers in pediatrics · 2024Article
- Article
- Article
- Autoimmune lymphoproliferative immunodeficiencies (ALPID) in childhood: breakdown of immune homeostasis and immune dysregulation.Molecular and cellular pediatrics · 2023Review
- Epstein-Barr virus-associated B-cell lymphoproliferative disorder meeting the definition of CAEBV B cell disease: a case report.BMC infectious diseases · 2023Article
- Successful treatment for diffuse large B-cell lymphoma in a Japanese adolescent with PIK3CD germ-line mutation: stem cell transplantation after reduced-intensity conditioning.Annals of hematology · 2022Article
- Article
- Druggable monogenic immune defects hidden in diverse medical specialties: Focus on overlap syndromes.World journal of clinical pediatrics · 2022Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Activated PI3Kδ Syndrome (APDS) is an inherited immune disorder caused by heterozygous, gain-of-function mutations in the genes encoding the phosphoinositide 3-kinase delta (PI3Kδ) subunits p110δ or p85δ. This recently described primary immunodeficiency disease (PID) is characterized by recurrent sinopulmonary infections, lymphoproliferation, and susceptibility to herpesviruses, with Epstein-Barr virus (EBV) infection being most notable. A broad range of PIDs having disparate, molecularly defined genetic etiology can cause susceptibility to EBV, lymphoproliferative disease, and lymphoma. Historically, PID patients with loss-of-function mutations causing defective cell-mediated cytotoxicity or antigen receptor signaling were found to be highly susceptible to pathological EBV infection. By contrast, the gain of function in PI3K signaling observed in APDS patients paradoxically renders these patients susceptible to EBV, though the underlying mechanisms are incompletely understood. At a cellular level, APDS patients exhibit deranged B lymphocyte development and defects in class switch recombination, which generally lead to defective immunoglobulin production. Moreover, APDS patients also demonstrate an abnormal skewing of T cells toward terminal effectors with short telomeres and senescence markers. Here, we review APDS with a particular focus on how the altered lymphocyte biology in these patients may confer EBV susceptibility.
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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.