ArticleEuropean journal of immunology2011
DOCK8 is essential for T-cell survival and the maintenance of CD8+ T-cell memory.
Article in European journal of immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 114 citations in OpenAlex.
- Autosomal recessive phosphoglucomutase 3 (PGM3) mutations link glycosylation defects to atopy, immune deficiency, autoimmunity, and neurocognitive impairment.The Journal of allergy and clinical immunology · 2014Trial
- Dock8 regulates Th2 cell differentiation through ANXA1.Fundamental research · 2026Article
- Immune-related actinopathies at the cross-road of immunodeficiency, autoimmunity and autoinflammation.Nature reviews. Immunology · 2026Review
- DOCK8 in immune cells: roles and mechanisms.Frontiers in immunology · 2026Review
- Use of Single-Cell Data and scPagwas Analysis to Identify T Cell Subsets and Construct a Prognostic Model for Clear Cell Renal Cell Carcinoma.Human mutation · 2026Article
- Comprehensive αβ T-Cell Receptor Repertoire Analysis Reveals a Unique CD8+ TCR Landscape in DOCK8-Deficient Patients.Allergy · 2025Article
- DIAPH1-Deficiency is Associated with Major T, NK and ILC Defects in Humans.Journal of clinical immunology · 2024Article
- B cells require DOCK8 to elicit and integrate T cell help when antigen is limiting.Science immunology · 2024Article
- Ectopic expression of DOCK8 regulates lysosome-mediated pancreatic tumor cell invasion.Cell reports · 2023Article
- DOCK8 is essential for neutrophil mediated clearance of cutaneous S. aureus infection.Clinical immunology (Orlando, Fla.) · 2023Article
- Article
- Inborn Errors of Immunity: A Role for Functional Testing and Flow Cytometry in Aiding Clinical Diagnosis.The journal of allergy and clinical immunology. In practice · 2023Article
- Insights into the pathogenesis of allergic disease from dedicator of cytokinesis 8 deficiency.Current opinion in immunology · 2023Review
- Genetic pleiotropy between pulmonary function and age-related traits: The Long Life Family Study.The journals of gerontology. Series A, Biological sciences and medical sciences · 2022Article
- Non-additive QTL mapping of lactation traits in 124,000 cattle reveals novel recessive loci.Genetics, selection, evolution : GSE · 2022Article
- CRISPR/Cas-Based Gene Editing Strategies for DOCK8 Immunodeficiency Syndrome.Frontiers in genome editing · 2022Article
- Deciphering the role of DOCK8 in tumorigenesis by regulating immunity and the application of nanotechnology in DOCK8 deficiency therapy.Frontiers in pharmacology · 2022Review
- RHO GTPases: from new partners to complex immune syndromes.Nature reviews. Immunology · 2021Review
- Review
- Proteomics Profiling to Distinguish DOCK8 Deficiency From Atopic Dermatitis.Frontiers in allergy · 2021Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Deficiency in the guanine nucleotide exchange factor dedicator of cytokinesis 8 (DOCK8) causes a human immunodeficiency syndrome associated with recurrent sinopulmonary and viral infections. We have recently identified a DOCK8-deficient mouse strain, carrying an ethylnitrosourea-induced splice-site mutation that shows a failure to mature a humoral immune response due to the loss of germinal centre B cells. In this study, we turned to T-cell immunity to investigate further the human immunodeficiency syndrome and its association with decreased peripheral CD4(+) and CD8(+) T cells. Characterisation of the DOCK8-deficient mouse revealed T-cell lymphopenia, with increased T-cell turnover and decreased survival. Egress of mature CD4(+) thymocytes was reduced with increased migration of these cells to the chemokine CXCL12. However, despite the two-fold reduction in peripheral naïve T cells, the DOCK8-deficient mice generated a normal primary CD8(+) immune response and were able to survive acute influenza virus infection. The limiting effect of DOCK8 was in the normal survival of CD8(+) memory T cells after infection. These findings help to explain why DOCK8-deficient patients are susceptible to recurrent infections and provide new insights into how T-cell memory is sustained.
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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.