Evidence map›Paper›PMID 26874355›Full record

ReviewInternational immunology2016

CD4+ T-cell subsets in inflammatory diseases: beyond the Th1/Th2 paradigm.

Kiyoshi Hirahara, Toshinori Nakayama

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in International immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05570383 (Observation on the Efficacy of Sublingual Immunotherapy With Dust Mite Allergen for Perennial Allergic Rhinitis and the Mechanism of Action on ILCs With ILC1s and ILC2s and ILC3s), which is not on this map. Cited by 217 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
217citing papers in PubMed, 5 pooled it
20.7field-weighted citation impact, top 1% 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.

NCT05570383 phase2 / phase3unknown statusnot on this mapstarted 2022, after this paper: background citation

Observation on the Efficacy of Sublingual Immunotherapy With Dust Mite Allergen for Perennial Allergic Rhinitis and the Mechanism of Action on ILCs With ILC1s and ILC2s and ILC3s

TypeinterventionalSponsorPeople's Hospital of Anshun City of Guizhou ProvinceRan2022 to 2024Enrolled60ConditionsAllergic RhinitisArmsDust mite drops (trade name: Changdi, Zhejiang Tawu Biotechnology Co. Ltd.).
3 · Its place in the literature

Who cites it

217 citing papers in PubMed, 5 syntheses or guidelines pooled it, 405 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  5. Pooled it
  6. Trial
  7. A phenotypically and functionally distinct human TScience translational medicine · 2017
    Trial
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Regulation of mCell biology and toxicology · 2026
    Review
  14. Review
  15. Review
  16. The Neuroimmunology of Autism.Molecular neurobiology · 2025
    Review
  17. Article
  18. Observational
  19. Review
  20. Review

157 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Kiyoshi HiraharaDepartment of Advanced Allergology of the Airway, Graduate School of Medicine, Chiba University, 1-8-1 Inohana Chuo-ku, Chiba 260-8670, Japan Department of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana Chuo-ku, Chiba 260-8670, Japan.
Toshinori NakayamaDepartment of Immunology, Graduate School of Medicine, Chiba University, 1-8-1 Inohana Chuo-ku, Chiba 260-8670, Japan AMED-CREST, The Japan Agency for Medical Research and Development (AMED), 1-8-1 Inohana Chuo-ku, Chiba 260-8670, Japan tnakayama@faculty.chiba-u.jp.
Chiba University · JPJapan Agency for Medical Research and Development · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD4(+)T cells are crucial for directing appropriate immune responses during host defense and for the pathogenesis of inflammatory diseases. In addition to the classical biphasic model of differentiation of T-helper 1 (Th1) and Th2 cells, unexpected increases in the numbers of CD4(+)T-cell subsets, including Th17, Th9, T follicular-helper (Tfh) and T-regulatory (Treg) cells, have been recognized. In the present review, we focus on how these various T-helper cell subsets contribute to the pathogenesis of immune-mediated inflammatory diseases. In particular, we focus on multiple sclerosis, psoriasis and asthma as typical model diseases in which multiple T-helper cell subsets have recently been suggested to play a role. We will also discuss various unique sub-populations of T-helper cells that have been identified. First, we will introduce the heterogeneous T-helper cell subsets, which are classified by their simultaneous expression of multiple key transcription factors. We will also introduce different kinds of memory-type Th2 cells, which are involved in the pathogenesis of chronic type-2 immune-related diseases. Finally, we will discuss the molecular mechanisms underlying the generation of the plasticity and heterogeneity of T-helper cell subsets. The latest progress in the study of T-helper cell subsets has forced us to reconsider the etiology of immune-mediated inflammatory diseases beyond the model based on the Th1/Th2 balance. To this end, we propose another model--the pathogenic T-helper population disease-induction model--as a possible mechanism for the induction and/or persistence of immune-mediated inflammatory diseases.

Indexed as

AnimalsCD4-Positive T-LymphocytesEpigenesis, GeneticGene Expression RegulationHost-Pathogen InteractionsHumansImmunologic MemoryInflammationTh1 CellsTh2 CellsT-Lymphocyte Subsetsepigeneticsmemory Th2 cellspathogenic Th2 (Tpath2) cellsT-cell plasticityTh1/Th2 paradigm

Identifiers

PMID26874355
PMCPMC4889886
OpenAlexW2267931422

What OpenQuestion holds

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Registered trials

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.