ArticleBlood2013
DOCK8 is critical for the survival and function of NKT cells.
Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed, 74 citations in OpenAlex.
- 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
- Comprehensive αβ T-Cell Receptor Repertoire Analysis Reveals a Unique CD8+ TCR Landscape in DOCK8-Deficient Patients.Allergy · 2025Article
- Article
- DOCK2 Deficiency Causes Defects in Antiviral T-Cell Responses and Impaired Control of Herpes Simplex Virus Infection.The Journal of infectious diseases · 2024Article
- B cells require DOCK8 to elicit and integrate T cell help when antigen is limiting.Science immunology · 2024Article
- Idiopathic non-cirrhotic portal hypertension in a patient with Talaromyces marneffei infection: a case report.BMC infectious diseases · 2023Article
- Mapping the splicing landscape of the human immune system.Frontiers in immunology · 2023Article
- Deciphering the role of DOCK8 in tumorigenesis by regulating immunity and the application of nanotechnology in DOCK8 deficiency therapy.Frontiers in pharmacology · 2022Review
- CRISPR/Cas-Based Gene Editing Strategies for DOCK8 Immunodeficiency Syndrome.Frontiers in genome editing · 2022Article
- Case Report: DOCK8 Deficiency Without Hyper-IgE in a Child With a Large Deletion.Frontiers in pediatrics · 2021Article
- DOCK8 deficiency diminishes thymic T-regulatory cell development but not thymic deletion.Clinical & translational immunology · 2021Article
- Ascorbic acid promotes the reproductive function of porcine immature Sertoli cells through transcriptome reprogramming.Theriogenology · 2020Article
- [Diffuse large B-cell lymphoma in a patient with hyper-IgE syndrome: a case report and literature review].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2020Review
- DOCK family proteins: key players in immune surveillance mechanisms.International immunology · 2020Review
- DOCK8 is expressed in microglia, and it regulates microglial activity during neurodegeneration in murine disease models.The Journal of biological chemistry · 2019Article
- Hematopoietic stem cell transplant effectively rescues lymphocyte differentiation and function in DOCK8-deficient patients.JCI insight · 2019Article
- Insights into immunity from clinical and basic science studies of DOCK8 immunodeficiency syndrome.Immunological reviews · 2019Review
- The ins and outs of type I iNKT cell development.Molecular immunology · 2019Review
- Human hyper-IgE syndrome: singular or plural?Mammalian genome : official journal of the International Mammalian Genome Society · 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 11 institutions in 3 countries.
Funding
Abstract
Patients with the dedicator of cytokinesis 8 (DOCK8) immunodeficiency syndrome suffer from recurrent viral and bacterial infections, hyper-immunoglobulin E levels, eczema, and greater susceptibility to cancer. Because natural killer T (NKT) cells have been implicated in these diseases, we asked if these cells were affected by DOCK8 deficiency. Using a mouse model, we found that DOCK8 deficiency resulted in impaired NKT cell development, principally affecting the formation and survival of long-lived, differentiated NKT cells. In the thymus, DOCK8-deficient mice lack a terminally differentiated subset of NK1.1(+) NKT cells expressing the integrin CD103, whereas in the liver, DOCK8-deficient NKT cells express reduced levels of the prosurvival factor B-cell lymphoma 2 and the integrin lymphocyte function-associated antigen 1. Although the initial NKT cell response to antigen is intact in the absence of DOCK8, their ongoing proliferative and cytokine responses are impaired. Importantly, a similar defect in NKT cell numbers was detected in DOCK8-deficient humans, highlighting the relevance of the mouse model. In conclusion, our data demonstrate that DOCK8 is required for the development and survival of mature NKT cells, consistent with the idea that DOCK8 mediates survival signals within a specialized niche. Accordingly, impaired NKT cell numbers and function are likely to contribute to the susceptibility of DOCK8-deficient patients to recurrent infections and malignant disease.
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.