ReviewJournal of clinical immunology2018
The Autoimmune Lymphoproliferative Syndrome with Defective FAS or FAS-Ligand Functions.
Review in Journal of clinical immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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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.
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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.
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Who cites it
44 citing papers in PubMed, 86 citations in OpenAlex.
- CMTM6 suppresses cell-surface expression of death receptor FAS in mice but not in humans.EMBO reports · 2026Article
- Lymphoproliferation in Inborn Errors of Immunity: Mechanisms, Manifestations and Clinical Management, with a Focus on ALPID.ImmunoTargets and therapy · 2026Review
- Immune system, inflammatory response, and regulated cell death in breast cancer research (Review).Oncology reports · 2026Review
- Review
- A Novel Cause of CIDP: Homozygous Hotspot Mutation, c.793 C > T in CASP8 Gene.Journal of clinical immunology · 2025Review
- Evolutionary regulation of human Fas ligand (CD95L) by plasmin in solid cancer immunotherapy.Nature communications · 2025Article
- FLIPProceedings of the National Academy of Sciences of the United States of America · 2025Article
- How (Ultra-)Rare Gene Variants Improve Our Understanding of More Common Autoimmune and Inflammatory Diseases.ACR open rheumatology · 2025Review
- Article
- Case Report: Clinical, molecular, and functional characterization of autoimmune lymphoproliferative syndrome-a family study with a multimodal diagnosis.Frontiers in pediatrics · 2025Article
- Novel Compound Heterozygous Variants in the FAS Gene Lead to Fetal Onset of Autoimmune Lymphoproliferative Syndrome (ALPS).Journal of clinical immunology · 2024Article
- Caspase-8 in inflammatory diseases: a potential therapeutic target.Cellular & molecular biology letters · 2024Review
- Identification of necroptosis-related genes in ankylosing spondylitis by bioinformatics and experimental validation.Journal of cellular and molecular medicine · 2024Article
- Study of the potential role of CASPASE-10 mutations in the development of autoimmune lymphoproliferative syndrome.Cell death & disease · 2024Article
- Autoimmune lymphoproliferative immunodeficiencies (ALPIDs): A proposed approach to redefining ALPS and other lymphoproliferative immune disorders.The Journal of allergy and clinical immunology · 2024Review
- Phenotypic Variability in PRKCD: a Review of the Literature.Journal of clinical immunology · 2023Review
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Too much of a good thing: a review of primary immune regulatory disorders.Frontiers in immunology · 2023Review
- Case report: Neonatal autoimmune lymphoproliferative syndrome with a novel pathogenic homozygousFrontiers in pediatrics · 2023Article
- Genetics of Immune Dysregulation and Cancer Predisposition: Two Sides of the Same Coin.Clinical and experimental immunology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The autoimmune lymphoproliferative syndrome (ALPS) is a non-malignant and non-infectious uncontrolled proliferation of lymphocytes accompanied by autoimmune cytopenia. The genetic etiology of the ALPS was described in 1995 by the discovery of the FAS gene mutations. The related apoptosis defect accounts for the accumulation of autoreactive lymphocytes as well as for specific clinical and biological features that distinguish the ALPS-FAS from other monogenic defects of this apoptosis pathway, such as FADD and CASPASE 8 deficiencies. The ALPS-FAS was the first description of a monogenic cause of autoimmunity, but its non-Mendelian expression remained elusive until the description of somatic and germline mutations in ALPS patients. The recognition of these genetic diseases brought new information on the role of this apoptotic pathway in controlling the adaptive immune response in humans.
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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.