ReviewGenes & diseases2020
Leukocyte adhesion defect: Where do we stand circa 2019?
Review in Genes & diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
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
27 citing papers in PubMed, 45 citations in OpenAlex.
- Structural basis of kindlin-3 in leukocyte adhesion deficiency III.Journal of thrombosis and haemostasis : JTH · 2026Article
- Leukocyte Adhesion Deficiency in a 42-Day-Old Infant: A Case Report.Clinical case reports · 2026Article
- Viral Prognosis Using Proteomics.Advances in experimental medicine and biology · 2026Review
- RhoA GAP Myo9b regulates β2-integrin activity and neutrophil recruitment during murine acute kidney injury.Blood · 2025Article
- Article
- A novel ITGB2 variant in a patient with severe recurrent pyoderma gangrenosum-like lesions and underlying leukocyte adhesion deficiency type I: case report and literature review.Archives of dermatological research · 2025Review
- GATA1-deficient human pluripotent stem cells generate neutrophils with improved antifungal immunity that is mediated by the integrin CD18.PLoS pathogens · 2025Article
- Article
- Sequence variants underlying severe combined immunodeficiency and leukocyte adhesion deficiency type 1 in six consanguineous families.Immunogenetics · 2024Article
- GATA1-deficient human pluripotent stem cells generate neutrophils with improved antifungal immunity that is mediated by the integrin CD18.bioRxiv : the preprint server for biology · 2024Article
- Analysis of Clinical, Immunological and Molecular Features of Leukocyte Adhesion Deficiency Type I in Egyptian Children.Journal of clinical immunology · 2024Article
- DualFrontiers in immunology · 2024Article
- SKAP2 acts downstream of CD11b/CD18 and regulates neutrophil effector function.Frontiers in immunology · 2024Article
- Rare and heterogeneous manifestations of leucocyte adhesion deficiency type 1: report of two cases with diagnostic dilemmas and novel ITGB2 mutation.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2023Article
- Turning universal O into rare Bombay type blood.Nature communications · 2023Article
- Organization, dynamics and mechanoregulation of integrin-mediated cell-ECM adhesions.Nature reviews. Molecular cell biology · 2023Review
- Selectin-Mediated Signaling-Shedding Light on the Regulation of Integrin Activity in Neutrophils.Cells · 2022Review
- A genome-wide association study in a large community-based cohort identifies multiple loci associated with susceptibility to bacterial and viral infections.Scientific reports · 2022Article
- NovelBioMed research international · 2022Article
- Expression of the phagocytic receptors αFrontiers in immunology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Migration of polymorphonuclear leukocytes from bloodstream to the site of inflammation is an important event required for surveillance of foreign antigens. This trafficking of leukocytes from bloodstream to the tissue occurs in several distinct steps and involves several adhesion molecules. Defect in adhesion of leukocytes to vascular endothelium affecting their subsequent migration to extravascular space gives rise to a group of rare primary immunodeficiency diseases (PIDs) known as Leukocyte Adhesion Defects (LAD). Till date, four classes of LAD are discovered with LAD I being the most common form. LAD I is caused by loss of function of common chain, cluster of differentiation (CD)18 of β2 integrin family. These patients suffer from life-threatening bacterial infections and in its severe form death usually occurs in childhood without bone marrow transplantation. LAD II results from a general defect in fucose metabolism. These patients suffer from less severe bacterial infections and have growth and mental retardation. Bombay blood group phenotype is also observed in these patients. LAD III is caused by abnormal integrin activation. LAD III patients suffer from severe bacterial and fungal infections. Patients frequently show delayed detachment of umbilical cord, impaired wound healing and increased tendency to bleed. LAD IV is the most recently described class. It is caused by defects in β2 and α4β1 integrins which impairs lymphocyte adhesion. LAD IV patients have monogenic defect in cystic-fibrosis-transmembrane-conductance-regulator (CFTR) gene, resulting in cystic fibrosis. Pathophysiology and genetic etiology of all LAD syndromes are discussed in detail in this paper.
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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.