Evidence map›Paper›PMID 26456931›Full record

ArticleImmunology2016

Expression of activation-induced cytidine deaminase enhances the clearance of pneumococcal pneumonia: evidence of a subpopulation of protective anti-pneumococcal B1a cells.

Natsuo Yamamoto, Steven M Kerfoot, Andrew T Hutchinson, Charles S Dela Cruz, Naomi Nakazawa, Marian Szczepanik, Monika Majewska-Szczepanik, Katarzyna Nazimek, Noboru Ohana, Krzysztof Bryniarski and 4 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 20% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. IL-21-dependent Ly6CCell death discovery · 2025
    Article
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  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Integrative Physiology of Pneumonia.Physiological reviews · 2018
    Review
  13. Article
  14. Corrigendum.Immunology · 2017
    Article
  15. Review
  16. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 3 countries.

Natsuo YamamotoSection of Allergy and Clinical Immunology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
Steven M KerfootSection of Allergy and Clinical Immunology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
Andrew T HutchinsonSection of Allergy and Clinical Immunology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
Charles S Dela CruzSection of Allergy and Clinical Immunology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
Naomi NakazawaDepartment of Infection Control, Fukushima Medical University, Hikarigaoka, Japan.
Marian SzczepanikSection of Allergy and Clinical Immunology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
Monika Majewska-SzczepanikSection of Allergy and Clinical Immunology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
Katarzyna NazimekSection of Allergy and Clinical Immunology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
Noboru OhanaDepartment of Infection Control, Fukushima Medical University, Hikarigaoka, Japan.
Krzysztof BryniarskiSection of Allergy and Clinical Immunology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
Tsutomu MoriDepartment of Infection Control, Fukushima Medical University, Hikarigaoka, Japan.
Masamichi MuramatsuDepartment of Molecular Genetics, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan.
Keiji KanemitsuDepartment of Infection Control, Fukushima Medical University, Hikarigaoka, Japan.
Philip W AskenaseSection of Allergy and Clinical Immunology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
Yale University · USFukushima Medical University · JPKanazawa University · JP

Funding

SOC CoreU54DA036134 · NIDA · BAYLOR COLLEGE OF MEDICINE · PI GALAS, DAVID J., GERSTEIN, MARK BENDER · 2013 to 2018
$15.0M
Host-Pneumococcal Interaction in the LungR01HL126094 · NHLBI · YALE UNIVERSITY · PI DELA CRUZ, CHARLES S · 2015 to 2019
$2.1M
NHLBI NIH HHS R01 HL126094NIAID NIH HHS AI-05981NIAID NIH HHS AI-07174NIAID NIH HHS AI-076366NIAID NIH HHS AI-1053786NIDA NIH HHS U54 DA036134NIDA NIH HHS U54-DA036134
6 · The paper itself

Abstract

We describe a protective early acquired immune response to pneumococcal pneumonia that is mediated by a subset of B1a cells. Mice deficient in B1 cells (xid), or activation-induced cytidine deaminase (AID(-/-) ), or invariant natural killer T (iNKT) cells (Jα18(-/-) ), or interleukin-13 (IL-13(-/-) ) had impaired early clearance of pneumococci in the lung, compared with wild-type mice. In contrast, AID(-/-) mice adoptively transferred with AID(+/+) B1a cells, significantly cleared bacteria from the lungs as early as 3 days post infection. We show that this early bacterial clearance corresponds to an allergic contact sensitivity-like cutaneous response, probably due to a subpopulation of initiating B1a cells. In the pneumonia model, these B1a cells were found to secrete higher affinity antigen-specific IgM. In addition, as in contact sensitivity, iNKT cells were required for the anti-pneumococcal B1a cell initiating response, probably through early production of IL-13, given that IL-13(-/-) mice also failed to clear infection. Our study is the first to demonstrate the importance of AID in generating an appropriate B1a cell response to pathogenic bacteria. Given the antibody affinity and pneumonia resistance data, natural IgM produced by conventional B1a cells are not responsible for pneumonia clearance compared with the AID-dependent subset.

Indexed as

Adaptive ImmunityPhagocytosisAdoptive TransferAgammaglobulinaemia Tyrosine KinaseAICDA (Activation-Induced Cytidine Deaminase)AnimalsAntigens, BacterialB-LymphocytesComplement ActivationCytidine DeaminaseCytokinesDermatitis, ContactDisease Models, AnimalGenotypeImmunoglobulin MInterleukin-13Agammaglobulinaemia Tyrosine KinaseAICDA (Activation-Induced Cytidine Deaminase)Antigens, BacterialBtk protein, mouseCytidine DeaminaseCytokinesImmunoglobulin MInterleukin-13Protein-Tyrosine Kinasesactivation-induced cytidine deaminaseB1a cellsIgM antibodyinterleukin-13invariant natural killer T cellspneumococcal pneumonia

Identifiers

PMID26456931
PMCPMC4693878
OpenAlexW1854950894

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.