Evidence map›Paper›PMID 38781720›Full record

ReviewCurrent opinion in immunology2024

In search of a function for human type III interferons: insights from inherited and acquired deficits.

Qian Zhang, Kai Kisand, Yi Feng, Darawan Rinchai, Emmanuelle Jouanguy, Aurélie Cobat, Jean-Laurent Casanova, Shen-Ying Zhang

Abstract readReview
In one paragraph

Review in Current opinion in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Powassan Virus NS5 Antagonizes TYK2-Mediated Immune Signaling Pathways.bioRxiv : the preprint server for biology · 2026
    Article
  2. Article
  3. Review
  4. The role of interferon regulatory factors in atherosclerosis.Frontiers in cardiovascular medicine · 2025
    Review
  5. Review
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

8 authors.

Qian ZhangSt. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, USA; Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, Paris, France; Paris Cité University, Imagine Institute, Paris, France. Electronic address: qzhang02@rockefeller.edu.
Kai KisandInstitute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia.
Yi FengSt. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, USA.
Darawan RinchaiSt. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, USA.
Emmanuelle JouanguySt. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, USA; Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, Paris, France; Paris Cité University, Imagine Institute, Paris, France.
Aurélie CobatSt. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, USA; Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, Paris, France; Paris Cité University, Imagine Institute, Paris, France.
Jean-Laurent CasanovaSt. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, USA; Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, Paris, France; Paris Cité University, Imagine Institute, Paris, France; Department of Pediatrics, Necker Hospital for Sick Children, AP-HP, Paris, France; Howard Hughes Medical Institute, New York, USA.
Shen-Ying ZhangSt. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, USA; Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, Paris, France; Paris Cité University, Imagine Institute, Paris, France.

Funding

Developing, Demonstrating, and Disseminating Innovative Programs to Achieve Translational SuccessUL1TR001866 · NCATS · ROCKEFELLER UNIVERSITY · PI COLLER, BARRY, KRUEGER, JAMES G · 2016 to 2025
$40.6M
Pharmacology & ImmunoPathology (PIP) CoreU19AI162568 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI EHRT, SABINE · 2021 to 2025
$13.0M
Monogenic basis of resistance to SARS-CoV2 and predisposition to severe COVID-19R01AI088364 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI Jean-Laurent Casanova, Shen-Ying Zhang · 2010 to 2026
$8.7M
Genome-wide search for inborn errors of IL-17 immunity underlying chronic mucocutaneous candidiasisR01AI127564 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI Jean-Laurent Casanova · 2017 to 2026
$4.8M
Inborn errors of immunity in patients with life-threatening COVID-19R01AI163029 · NIAID · ROCKEFELLER UNIVERSITY · PI CASANOVA, JEAN-LAURENT, ZHANG, QIAN · 2021 to 2025
$3.7M
Genome-Wide Dissection of Mendelian Susceptibility to Mycobacterial DiseaseR01AI095983 · NIAID · ROCKEFELLER UNIVERSITY · PI BUSTAMANTE, JACINTA, CASANOVA, JEAN-LAURENT · 2021 to 2025
$2.5M
Single gene inborn errors of immunity underlying SARS-CoV-2-related multisystem inflammatory syndrome in children: a new approach to tackle a seemingly old puzzleR21AI160576 · NIAID · ROCKEFELLER UNIVERSITY · PI ZHANG, SHEN-YING · 2022 to 2023
$466k
NCATS NIH HHS UL1 TR001866NIAID NIH HHS R01 AI088364NIAID NIH HHS R01 AI095983NIAID NIH HHS R01 AI127564NIAID NIH HHS R01 AI163029NIAID NIH HHS R21 AI160576NIAID NIH HHS U19 AI162568
6 · The paper itself

Abstract

The essential and redundant functions of human type I and II interferons (IFNs) have been delineated over the last three decades by studies of patients with inborn errors of immunity or their autoimmune phenocopies, but much less is known about type III IFNs. Patients with cells that do not respond to type III IFNs due to inherited IL10RB deficiency display no overt viral disease, and their inflammatory disease phenotypes can be explained by defective signaling via other interleukine10RB-dependent pathways. Moreover, patients with inherited deficiencies of interferon-stimulated gene factor 3 (ISGF-3) (STAT1, STAT2, IRF9) present viral diseases also seen in patients with inherited deficiencies of the type I IFN receptor (IFNAR1/2). Finally, patients with autoantibodies neutralizing type III IFNs have no obvious predisposition to viral disease. Current findings thus suggest that type III IFNs are largely redundant in humans. The essential functions of human type III IFNs, particularly in antiviral defenses, remain to be discovered.

Indexed as

Interferon LambdaInterferonsVirus DiseasesAnimalsHumansInterferon-Stimulated Gene Factor 3, gamma SubunitInterleukin-10 Receptor beta SubunitSignal TransductionSTAT1 Transcription FactorSTAT2 Transcription FactorIL10RB protein, humanInterferon LambdaInterferonsInterferon-Stimulated Gene Factor 3, gamma SubunitInterleukin-10 Receptor beta SubunitSTAT1 Transcription FactorSTAT2 Transcription Factor

Identifiers

PMID38781720
PMCPMC11209856

What OpenQuestion holds

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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.