ReviewJournal of clinical immunology2023
Phenotypic Variability in PRKCD: a Review of the Literature.
Review 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.
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
7 citing papers in PubMed, 11 citations in OpenAlex.
- Human inborn errors of the phagocyte respiratory burst: Chronic granulomatous disease and beyond.Journal of human immunity · 2026Article
- Expanding the scope of PI3K-δ inhibition: Leniolisib treatment in PRKCD deficiency.Journal of human immunity · 2026Article
- Identification of marker genes associated with oxidative stress in hypertrophic cardiomyopathy using bioinformatics analysis and experimental validation.Scientific reports · 2025Article
- Primary immunodeficiency as a cause of immune-mediated kidney diseases.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024Review
- Diagnosis of Chronic Granulomatous Disease: Strengths and Challenges in the Genomic Era.Journal of clinical medicine · 2024Review
- Mendelian Causes of Autoimmunity: the Lupus Phenotype.Journal of clinical immunology · 2024Review
- Kinome and phosphoproteome reprogramming underlies the aberrant immune responses in critically ill COVID-19 patients.Clinical proteomics · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeProtein kinase C δ (PKCδ) deficiency is a rare genetic disorder identified as a monogenic cause of systemic lupus erythematosus in 2013. Since the first cases were described, the phenotype has expanded to include children presenting with autoimmune lymphoproliferative syndrome-related syndromes and infection susceptibility similar to chronic granulomatous disease or combined immunodeficiency. We review the current published data regarding the pathophysiology, clinical presentation, investigation and management of PKCδ deficiency.
methodsLiterature review was performed using MEDLINE.
resultsTwenty cases have been described in the literature with significant heterogeneity.
conclusionThe variation in clinical presentation delineates the broad and critical role of PKCδ in immune tolerance and effector functions against pathogens.
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.