ArticleJournal of clinical immunology2023
Multiple Immune Defects in Two Patients with Novel DOCK2 Mutations Result in Recurrent Multiple Infection Including Live Attenuated Virus Vaccine.
Article in Journal of clinical immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Heterozygous variants in DOCK2 leading to susceptibility to viral illnesses.The Journal of allergy and clinical immunology · 2026Article
- Association of the Dedicator of Cytokinesis 2 (DOCK2) Gene Polymorphisms with COVID-19 and Plasma LDH, AST, ALT, and Ferritin Levels.Biomolecules · 2026Article
- Mucosal Inflammation Shapes Human Neutrophil States in Tissue and Circulation.bioRxiv : the preprint server for biology · 2026Article
- DOCK2 Deficiency and GATA2 Haploinsufficiency Can Underlie Critical Coronavirus Disease 2019 (COVID-19) Pneumonia.Journal of clinical immunology · 2025Article
- Two cases of combined immunodeficiency with ITPR3 mutations presenting with life-threatening severe EBV-associated hemophagocytic lymphohistiocytosis.Frontiers in immunology · 2025Article
- Fluoxetine Successfully Treats Intracranial Enterovirus E18 Infection in a Patient with CD79a Deficiency Arising from Segmental Uniparental Disomy of Chromosome 19.Journal of clinical immunology · 2024Article
- Case report: A cyclic neutropenia patient withFrontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The dedicator of cytokinesis 2(DOCK2) protein, an atypical guanine nucleotide exchange factor (GEFs), is a member of the DOCKA protein subfamily. DOCK2 protein deficiency is characterized by early-onset lymphopenia, recurrent infections, and lymphocyte dysfunction, which was classified as combined immune deficiency with neutrophil abnormalities as well. The only cure is hematopoietic stem cell transplantation. Here, we report two patients harboring four novel DOCK2 mutations associated with recurrent infections including live attenuated vaccine-related infections. The patient's condition was partially alleviated by symptomatic treatment or intravenous immunoglobulin. We also confirmed defects in thymic T cell output and T cell proliferation, as well as aberrant skewing of T/B cell subset TCR-Vβ repertoires. In addition, we noted neutrophil defects, the weakening of actin polymerization, and BCR internalization under TCR/BCR activation. Finally, we found that the DOCK2 protein affected antibody affinity although with normal total serum immunoglobulin. The results reported herein expand the clinical phenotype, the pathogenic DOCK2 mutation database, and the immune characteristics of DOCK2-deficient patients.
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Registered trials
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