Evidence map›Paper›PMID 38773012›Full record

ArticleJournal of clinical immunology2024

Variable Syndromic Immunodeficiency in Patients with Biallelic PRIM1 Mutations.

Vasil Toskov, Petra Kaiser-Labusch, Min Ae Lee-Kirsch, PRIM1 study group, Stephan Ehl, Oliver Wegehaupt

Abstract readCase Reports
In one paragraph

Article in Journal of clinical immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Vasil ToskovClinic of Pediatric Hematology, Oncology and Stem Cell Transplantation, Medical Center, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Petra Kaiser-LabuschProf. Hess Children's Hospital, Klinikum Bremen-Mitte, Gesundheit Nord gGmbH, Bremen, Germany.
Min Ae Lee-KirschDepartment of Pediatrics, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
PRIM1 study group
Stephan EhlInstitute for Immunodeficiency, Center for Chronic Immunodeficiency (CCI), Medical Center, Faculty of Medicine, University of Freiburg, Breisacher Str. 115, 79106, Freiburg, Germany. stephan.ehl@uniklinik-freiburg.de.
Oliver WegehauptClinic of Pediatric Hematology, Oncology and Stem Cell Transplantation, Medical Center, Faculty of Medicine, University of Freiburg, Freiburg, Germany. oliver.wegehaupt@uniklinik-freiburg.de.ORCID 0000-0002-9391-0761

Funding

BMBF-funded German Auto-Immunity Network (GAIN) 197 01GM1910ADeutsche Forschungsgemeinschaft (DFG, German Research Foundation) CIBSS-EXC-21899-Project ID 390939984Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) CRC237 369799452/A06Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) CRC237 369799452/B21 and CRC237 369799452/A11
6 · The paper itself

Abstract

Mutations in genes of the DNA polymerase complex have been linked to impaired immunological function next to distinct syndromic features. Biallelic mutations in PRIM1 are associated with a primordial dwarfism syndrome with variable hypogammaglobulinemia. The disease is mostly lethal in infancy due to pulmonary infections as well as hepatic cirrhosis. We studied 3 novel patients with PRIM1-deficiency with a focus on immunological consequences. All three shared dysmorphic features including a prominent forehead, triangular face and bilateral cryptorchidism. P1 carried the novel homozygous PRIM1 splice variant c.103+2T>G, allowing residual protein expression and associated with a mild clinical phenotype. P2 and P3 carried the known homozygous variant c.638+36C>G and died in infancy. Paradoxically, B cell lymphopenia was most pronounced in P1. No other significant lymphocyte abnormalities were detected. Interestingly, all 3 patients showed variable, but intermittently excessive Type I interferon signatures. In summary, the B-cell deficiency in PRIM1-deficiency is markedly variable and the severity of syndromic manifestations is not predictive of the immunological phenotype. We highlight a potential contribution of pathological type I interferon activation to disease pathogenesis which warrants further investigations.

Indexed as

AllelesB-LymphocytesMutationChild, PreschoolDNA PrimaseFemaleHumansImmunologic Deficiency SyndromesInfantInterferon Type IMalePhenotypeDNA PrimaseInterferon Type IPRIM1 protein, humanagammaglobulinemiaB cell deficiencyimmunodeficiencyinterferonopathyPRIM1primordial dwarfismtype I interferon

Identifiers

PMID38773012
PMCPMC11108906

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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.