ArticleThe Journal of experimental medicine2012
Expansion of somatically reverted memory CD8+ T cells in patients with X-linked lymphoproliferative disease caused by selective pressure from Epstein-Barr virus.
Article in The Journal of experimental medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 67 citations in OpenAlex.
- Genetic Heterogeneity of Inborn Errors of Immunity Revealed by Whole-Genome Sequencing: Insights from a Russian Patient Cohort.International journal of molecular sciences · 2026Article
- Identifying genetic errors of immunity due to mosaicism.The Journal of experimental medicine · 2025Review
- Somatic mosaicism in genetic errors of immunity.The Journal of allergy and clinical immunology · 2025Review
- X-linked lymphoproliferative disease type 1: a clinical and genetic update.Frontiers in immunology · 2025Review
- Review
- Review
- Genome Editing With TALEN, CRISPR-Cas9 and CRISPR-Cas12a in Combination With AAV6 Homology Donor Restores T Cell Function for XLP.Frontiers in genome editing · 2022Article
- Leveraging Systems Immunology to Optimize Diagnosis and Treatment of Inborn Errors of Immunity.Frontiers in systems biology · 2022Article
- Review
- Genetic Mosaicism as a Cause of Inborn Errors of Immunity.Journal of clinical immunology · 2021Review
- COVID-19, varying genetic resistance to viral disease and immune tolerance checkpoints.Immunology and cell biology · 2021Review
- Lethal Infectious Diseases as Inborn Errors of Immunity: Toward a Synthesis of the Germ and Genetic Theories.Annual review of pathology · 2021Review
- Reversion Mosaicism in Primary Immunodeficiency Diseases.Frontiers in immunology · 2021Review
- The Natural History of X-Linked Lymphoproliferative Disease (XLP1): Lessons from a Long-Term Survivor.Case reports in immunology · 2020Article
- Somatic genetic rescue in Mendelian haematopoietic diseases.Nature reviews. Genetics · 2019Review
- Flow Cytometric-Based Analysis of Defects in Lymphocyte Differentiation and Function Due to Inborn Errors of Immunity.Frontiers in immunology · 2019Review
- Somatic alterations compromised molecular diagnosis of DOCK8 hyper-IgE syndrome caused by a novel intronic splice site mutation.Scientific reports · 2018Article
- Human hyper-IgE syndrome: singular or plural?Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Human genetics of infectious diseases: Unique insights into immunological redundancy.Seminars in immunology · 2018Review
- X-Linked Lymphoproliferative Disease Type 1: A Clinical and Molecular Perspective.Frontiers in immunology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 15 institutions in 4 countries.
Funding
Abstract
Patients with the primary immunodeficiency X-linked lymphoproliferative disease (XLP), which is caused by mutations in SH2D1A, are highly susceptible to Epstein-Barr virus (EBV) infection. Nonetheless, some XLP patients demonstrate less severe clinical manifestations after primary infection. SH2D1A encodes the adaptor molecule SLAM-associated protein (SAP), which is expressed in T and natural killer cells and is required for cytotoxicity against B cells, the reservoir for EBV. It is not known why the clinical presentation of XLP is so variable. In this study, we report for the first time the occurrence of somatic reversion in XLP. Reverted SAP-expressing cells resided exclusively within the CD8(+) T cell subset, displayed a CD45RA(-)CCR7(-) effector memory phenotype, and were maintained at a stable level over time. Importantly, revertant CD8(+) SAP(+) T cells, but not SAP(-) cells, proliferated in response to EBV and killed EBV-infected B cells. As somatic reversion correlated with EBV infection, we propose that the virus exerts a selective pressure on the reverted cells, resulting in their expansion in vivo and host protection against ongoing infection.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.