Evidence map›Paper›PMID 30635395›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2019

Lack of Ikaros Deregulates Inflammatory Gene Programs in T Cells.

Carolina Lyon de Ana, Ksenia Arakcheeva, Parul Agnihotri, Nicole Derosia, Susan Winandy

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Ikaros is a principal regulator of AireScience immunology · 2023
    Article
  11. Article
  12. Review
  13. Article
  14. CD4Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  15. Review
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  18. Article
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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

5 authors at 1 institution in 1 country.

Carolina Lyon de AnaDepartment of Pathology and Laboratory Medicine, Immunology Training Program, Boston University School of Medicine, Boston, MA 02118.ORCID 0000-0002-2964-1624
Ksenia ArakcheevaDepartment of Pathology and Laboratory Medicine, Immunology Training Program, Boston University School of Medicine, Boston, MA 02118.
Parul AgnihotriDepartment of Pathology and Laboratory Medicine, Immunology Training Program, Boston University School of Medicine, Boston, MA 02118.
Nicole DerosiaDepartment of Pathology and Laboratory Medicine, Immunology Training Program, Boston University School of Medicine, Boston, MA 02118.
Susan WinandyDepartment of Pathology and Laboratory Medicine, Immunology Training Program, Boston University School of Medicine, Boston, MA 02118 swinandy@bu.edu.ORCID 0000-0001-7804-9603
Boston University · US

Funding

RESEARCH TRAINING IN IMMUNOLOGYT32AI007309 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GUMMULURU, SURYARAM · 1988 to 2024
$7.4M
Elucidation of Ikaros function in peripheral T cell responses in vivoR21AI113522 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WINANDY, SUSAN M · 2016 to 2017
$452k
Defining programs of gene expression regulated by Ikaros in T cellsR03AI133228 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WINANDY, SUSAN M · 2018 to 2019
$165k
NIAID NIH HHS R03 AI133228NIAID NIH HHS R21 AI113522NIAID NIH HHS T32 AI007309
6 · The paper itself

Abstract

CD4 Th cells are organizers of the immune response, directing other immune cells to initiate and maintain effective humoral and cellular immunity. CD4 T cells differentiate into distinct Th effector or regulatory subsets in response to signals delivered to them during the course of infection. Ikaros is a transcription factor that is expressed in blood cells from the level of the hematopoietic stem cell. It is required for normal thymic T cell development and serves as a tumor suppressor, as lack of Ikaros in developing lymphoid cells results in leukemia. To study the role of Ikaros in CD4 T cell differentiation and function, an Ikaros conditional knockout mouse was developed such that Ikaros expression was deleted specifically in mature T cells, thus avoiding defects observed in germline Ikaros mutant mice. Using this model system, we have shown that in the absence of Ikaros, CD4 T cells are able to attain Th1, Th2, and Th17, but not inducible regulatory T, cell fates. However, they show enhanced expression of a cohort of proinflammatory cytokines, resulting in differentiation of Th17 cells with a phenotype that has been associated with autoimmunity and pathological inflammation. In addition, we define Ikaros as a repressor of the gene program associated with the response to type I IFNs, another key pathway whose deregulation is linked to autoimmunity. Taken together, these data definitively define Ikaros as a critical regulator at the center of the inflammatory response in T cells and highlight a potential role in suppressing autoimmunity.

Indexed as

AnimalsCD4-Positive T-LymphocytesFemaleIkaros Transcription FactorInflammationInterferon Type IMaleMiceMice, Inbred C57BLMice, KnockoutMutationIkaros Transcription FactorInterferon Type IZfpn1a1 protein, mouse

Identifiers

PMID30635395
PMCPMC6365004
OpenAlexW2908931313

What OpenQuestion holds

Textmetadata
LicenceTDM
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.