Evidence map›Paper›PMID 27481850›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

Accelerated Loss of TCR Repertoire Diversity in Common Variable Immunodeficiency.

Gabriel K Wong, David Millar, Sarah Penny, James M Heather, Punam Mistry, Nico Buettner, Jane Bryon, Aarnoud P Huissoon, Mark Cobbold

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

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  6. From thymus to tissues and tumors: A review of T-cell biology.The Journal of allergy and clinical immunology · 2023
    Review
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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

9 authors.

Gabriel K WongMedical Research Council Centre for Immune Regulation, University of Birmingham, Edgbaston B15 2TT, United Kingdom; West Midlands Primary Immunodeficiency Centre, Birmingham Heartlands Hospital, Birmingham B9 5SS, United Kingdom;ORCID 0000-0003-4987-4051
David MillarCancer Center, Massachusetts General Hospital, Boston MA 02114; Department of Medicine, Harvard Medical School, Charlestown, MA 02129;ORCID 0000-0002-0104-9303
Sarah PennyMedical Research Council Centre for Immune Regulation, University of Birmingham, Edgbaston B15 2TT, United Kingdom;
James M HeatherDivision of Infection and Immunity, University College London, London WC1E 6BT, United Kingdom; and.ORCID 0000-0002-1783-5181
Punam MistryMedical Research Council Centre for Immune Regulation, University of Birmingham, Edgbaston B15 2TT, United Kingdom;
Nico BuettnerMedical Research Council Centre for Immune Regulation, University of Birmingham, Edgbaston B15 2TT, United Kingdom;
Jane BryonRegional Genetics Laboratory, Birmingham Women's Hospital, Birmingham B15 2TG, United Kingdom.
Aarnoud P HuissoonWest Midlands Primary Immunodeficiency Centre, Birmingham Heartlands Hospital, Birmingham B9 5SS, United Kingdom;
Mark CobboldCancer Center, Massachusetts General Hospital, Boston MA 02114; Department of Medicine, Harvard Medical School, Charlestown, MA 02129; mcobbold@mgh.harvard.edu.ORCID 0000-0001-8931-4142

Funding

Wellcome Trust 099908
6 · The paper itself

Abstract

Although common variable immunodeficiency (CVID) has long been considered as a group of primary Ab deficiencies, growing experimental data now suggest a global disruption of the entire adaptive immune response in a segment of patients. Oligoclonality of the TCR repertoire was previously demonstrated; however, the manner in which it relates to other B cell and T cell findings reported in CVID remains unclear. Using a combination approach of high-throughput TCRβ sequencing and multiparametric flow cytometry, we compared the TCR repertoire diversity between various subgroups of CVID patients according to their B cell immunophenotypes. Our data suggest that the reduction in repertoire diversity is predominantly restricted to those patients with severely reduced class-switched memory B cells and an elevated level of CD21(lo) B cells (Freiburg 1a), and may be driven by a reduced number of naive T cells unmasking underlying memory clonality. Moreover, our data indicate that this loss in repertoire diversity progresses with advancing age far exceeding the expected physiological rate. Radiological evidence supports the loss in thymic volume, correlating with the decrease in repertoire diversity. Evidence now suggests that primary thymic failure along with other well-described B cell abnormalities play an important role in the pathophysiology in Freiburg group 1a patients. Clinically, our findings emphasize the integration of combined B and T cell testing to identify those patients at the greatest risk for infection. Future work should focus on investigating the link between thymic failure and the severe reduction in class-switched memory B cells, while gathering longitudinal laboratory data to examine the progressive nature of the disease.

Indexed as

Age FactorsB-LymphocytesCommon Variable ImmunodeficiencyFlow CytometryHigh-Throughput Nucleotide SequencingHumansImmunoglobulin Class SwitchingImmunologic MemoryImmunophenotypingLymphocyte DepletionMiddle AgedReceptors, Antigen, T-Cell, alpha-betaReceptors, Complement 3dThymus GlandT-LymphocytesReceptors, Antigen, T-Cell, alpha-betaReceptors, Complement 3d

Identifiers

PMID27481850
PMCPMC4991247

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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.