Evidence map›Paper›PMID 26407811›Full record

ArticleJournal of clinical immunology2015

Late-Onset Combined Immunodeficiency with a Novel IL2RG Mutation and Probable Revertant Somatic Mosaicism.

Yusuke Okuno, Akihiro Hoshino, Hideki Muramatsu, Nozomu Kawashima, Xinan Wang, Kenichi Yoshida, Taizo Wada, Masaharu Gunji, Tomoko Toma, Tamaki Kato and 14 more

Abstract readCase Reports
PubMed Publisher
In one paragraph

Article in Journal of clinical immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.4field-weighted citation impact, top 35% of its field
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

19 citing papers in PubMed, 28 citations in OpenAlex.

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  19. A NovelFrontiers in pediatrics · 2018
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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

24 authors at 8 institutions in 1 country.

Yusuke OkunoDepartment of Pediatrics, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Akihiro HoshinoDepartment of Pediatrics, Graduate School of Medicine, University of Toyama, Toyama, Japan.
Hideki MuramatsuDepartment of Pediatrics, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Nozomu KawashimaDepartment of Pediatrics, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Xinan WangDepartment of Pediatrics, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Kenichi YoshidaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Taizo WadaDepartment of Pediatrics, School of Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa, Japan.
Masaharu GunjiDepartment of Pathology, Japanese Red Cross Nagoya first Hospital, Nagoya, Japan.
Tomoko TomaDepartment of Pediatrics, School of Medicine, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa, Japan.
Tamaki KatoDepartment of Pediatrics, National Defense Medical College, Saitama, Japan.
Yuichi ShiraishiLaboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Atsuko IwataDepartment of Pediatrics, Aichi Medical University School of Medicine, Nagakute, Japan.
Toshinori HoriDepartment of Pediatrics, Aichi Medical University School of Medicine, Nagakute, Japan.
Toshiyuki KitohDepartment of Pediatrics, Aichi Medical University School of Medicine, Nagakute, Japan.
Kenichi ChibaLaboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Hiroko TanakaLaboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Masashi SanadaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Yoshiyuki TakahashiDepartment of Pediatrics, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Shigeaki NonoyamaDepartment of Pediatrics, National Defense Medical College, Saitama, Japan.
Masafumi ItoDepartment of Pathology, Japanese Red Cross Nagoya first Hospital, Nagoya, Japan.
Satoru MiyanoLaboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Seishi OgawaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Seiji KojimaDepartment of Pediatrics, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Hirokazu KaneganeDepartment of Pediatrics, Graduate School of Medicine, University of Toyama, Toyama, Japan. hkanegane.ped@tmd.ac.jp.
Nagoya University · JPThe University of Tokyo · JPAichi Medical University · JPKyoto University · JPKanazawa University · JPNational Defense Medical College · JPTokyo Medical and Dental University · JPUniversity of Toyama · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary immunodeficiency disease (PID) is caused by mutations of more than two hundred immunity-related genes. In addition to the heterogeneity of the diseases, the atypical presentation of each disease caused by hypomorphic mutations or somatic mosaicism makes genetic diagnosis challenging. Next-generation sequencing tests all genes simultaneously and has proven its innovative efficacy in genomics. We describe a male PID patient without any family history of immunodeficiency. This patient suffered from recurrent infections from 1 year of age. Laboratory analysis showed hypogammaglobulinemia. T, B, and NK cells were present, but the T cell proliferative response decreased. Whole-exome sequencing analysis identified an IL2RG p.P58T missense mutation. CD8(+) and CD56(+) cells showed revertant somatic mosaicism to the wild-type allele. A late-onset and atypical presentation of the X-linked severe combined immunodeficiency (X-SCID) phenotype might be associated with revertant somatic mosaicism in T and NK cells. This patient is the seventh reported case of X-SCID with revertant somatic mosaicism. His classical clinical management did not result in a molecular diagnosis because of the atypical presentation. The coverage that is provided by whole-exome sequencing of most PID genes effectively excluded differential diagnoses other than X-SCID. As next-generation sequencing becomes available in clinical practice, it will enhance our knowledge of PID and rescue currently undiagnosed patients.

Indexed as

Hematopoietic Stem Cell TransplantationAspergillusCD8-Positive T-LymphocytesChildChild, PreschoolDiagnosis, DifferentialDNA Mutational AnalysisFatal OutcomeGraft RejectionHumansImmunologic Deficiency SyndromesInfantInterleukin Receptor Common gamma SubunitInvasive Pulmonary AspergillosisJapanMaleIL2RG protein, humanInterleukin Receptor Common gamma SubunitCombined immunodeficiencyRevertant somatic mosaicismWhole-exome sequencingX-linked severe combined immunodeficiency

Identifiers

PMID26407811
OpenAlexW2467973839

What OpenQuestion holds

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Registered trials

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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.