Evidence map›Paper›PMID 28747343›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2017

The Development of Steady-State Activation Hubs between Adult LTi ILC3s and Primed Macrophages in Small Intestine.

Adam K Savage, Hong-Erh Liang, Richard M Locksley

Open access · greenAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. CD4 T-Cell Subsets and the Pathophysiology of Inflammatory Bowel Disease.International journal of molecular sciences · 2023
    Review
  7. ILCs-Crucial Players in Enteric Infectious Diseases.International journal of molecular sciences · 2022
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Spatial distribution of LTi-like cells in intestinal mucosa regulates type 3 innate immunity.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  17. Article
  18. Article
  19. Review
  20. Keeping time in group 3 innate lymphoid cells.Nature reviews. Immunology · 2020
    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

3 authors at 2 institutions in 1 country.

Adam K SavageHoward Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94158.ORCID 0000-0003-1913-5485
Hong-Erh LiangDepartment of Medicine, University of California, San Francisco, San Francisco, CA 94143; and.
Richard M LocksleyHoward Hughes Medical Institute, University of California, San Francisco, San Francisco, CA 94158; richard.locksley@ucsf.edu.
Howard Hughes Medical Institute · USUniversity of California, San Francisco · US

Funding

UCSF Nutrition Obesity Research CenterP30DK098722 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHRISTIAN VAISSE · 2015 to 2026
$14.6M
Initiation of allergic immunity by parasitesR01AI030663 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOCKSLEY, RICHARD M · 1991 to 2016
$5.7M
Parasite immunity orchestrated by type 2 immune cellsR01AI026918 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOCKSLEY, RICHARD M · 1988 to 2022
$3.8M
Epithelial chitinase and lung homeostasisR01HL128903 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LOCKSLEY, RICHARD M · 2015 to 2018
$1.6M
Howard Hughes Medical InstituteNHLBI NIH HHS R01 HL128903NIAID NIH HHS R01 AI026918NIAID NIH HHS R01 AI030663NIDDK NIH HHS P30 DK098722
6 · The paper itself

Abstract

Group 3 innate lymphoid cells (ILC3s) are important for intestinal health, particularly in controlling inflammation in response to epithelial dysregulation, but their role during homeostasis remains less well understood. We generated IL-22 reporter mice to assess production of this key cytokine by ILC3s in the small intestine during development and under basal conditions. Although IL-22 is produced by a variety of lymphocyte populations, constitutively high IL-22 expression was limited to lymphoid-tissue inducer (LTi) cells residing in lymph node-like structures in the gut called solitary intestinal lymphoid tissues (SILT). Constitutive IL-22 expression was dependent on the microbiota and MyD88 signaling, appeared upon weaning, and was present across the spectrum of SILT, including in cryptopatches. Activated SILT LTi cells colocalized with a rare subpopulation of activated macrophages constitutively positive for IL-12/23 p40 and capable of activating neonatal LTi cells in response to TLR stimulus. Thus, weaning leads to the organization of innate immune activation hubs at SILT that mature and are continuously sustained by signals from the microbiota. This functional and anatomic organization constitutes a significant portion of the steady-state IL-23/IL-22 axis.

Indexed as

AnimalsCell DifferentiationCells, CulturedImmunity, InnateInterleukin-12Interleukin-22Interleukin-23InterleukinsIntestine, SmallLymphocyte ActivationLymphocytesMacrophagesMiceMice, Inbred C57BLMice, TransgenicMicrobiotaInterleukin-12Interleukin-22Interleukin-23InterleukinsMyd88 protein, mouseMyeloid Differentiation Factor 88

Identifiers

PMID28747343
PMCPMC5568484
OpenAlexW2737385511

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.