Evidence map›Paper›PMID 26644324›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2016

A critical role of Dectin-1 in hypersensitivity pneumonitis.

Mari Higashino-Kameda, Toshiki Yabe-Wada, Shintaro Matsuba, Kazuya Takeda, Kazushi Anzawa, Takashi Mochizuki, Koichi Makimura, Shinobu Saijo, Yoichiro Iwakura, Hirohisa Toga and 1 more

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Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. How experimental models have unlocked hidden mechanisms of hypersensitivity pneumonitis.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. C-type lectins in immunity and homeostasis.Nature reviews. Immunology · 2018
    Review
  9. Review
  10. Article
  11. The Cell Biology of theFrontiers in cellular and infection microbiology · 2017
    Review
  12. Review
  13. Article
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

11 authors at 4 institutions in 1 country.

Mari Higashino-KamedaDepartment of Respiratory Medicine, Kanazawa Medical University, Uchinada, Ishikawa, Japan.
Toshiki Yabe-WadaDepartment of Immunology, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Ishikawa Prefecture, 920-0293, Japan.
Shintaro MatsubaDepartment of Immunology, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Ishikawa Prefecture, 920-0293, Japan.
Kazuya TakedaDepartment of Immunology, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Ishikawa Prefecture, 920-0293, Japan.
Kazushi AnzawaDepartment of Dermatology, Kanazawa Medical University, Uchinada, Ishikawa, Japan.
Takashi MochizukiDepartment of Dermatology, Kanazawa Medical University, Uchinada, Ishikawa, Japan.
Koichi MakimuraLaboratory of Space and Environmental Medicine, Teikyo University, Hachioji, Tokyo, Japan.
Shinobu SaijoDivision of Molecular Immunology, Medical Mycology Research Center, Chiba University, Chiba, Japan.
Yoichiro IwakuraCenter for Animal Disease Models, Research Institute for Biological Sciences, Tokyo University of Science, Noda, Chiba, Japan.
Hirohisa TogaDepartment of Respiratory Medicine, Kanazawa Medical University, Uchinada, Ishikawa, Japan.
Akira NakamuraDepartment of Immunology, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Ishikawa Prefecture, 920-0293, Japan. aki-n@kanazawa-med.ac.jp.
Kanazawa Medical University · JPChiba University · JPTeikyo University · JPTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

OBJECTIVES AND

designHypersensitivity pneumonitis (HP) is a pulmonary disease caused by repeated exposure to various aspiration antigens, including bacteria and fungi. Although TLRs are known to be required for the generation of HP triggered by bacteria, the significance of fungal receptors remains unclear. The present study aimed to investigate whether Dectin-1 and Dectin-2 contribute to the development of experimental HP triggered by the fungus Trichosporon asahii (T. asahii) that causes summer-type HP. MATERIALS AND

methodsWe investigated the binding between Dectin-Fc protein and T. asahii by a dot blot assay. We performed the histological and flow cytometric analysis in the HP model using Dectin-1-deficient (Dectin-1(-/-)) and Dectin-2(-/-) mice. We also investigated Th17/Th1 responses in lung cells, and measured an IL-17-promoting cytokine IL-23 from bone marrow-derived dendritic cells (BMDCs) by ELISA.

resultsDectin-1 bound more strongly to T. asahii than Dectin-2. Dectin-1(-/-) mice barely developed HP, whereas both wild-type mice and Dectin-2(-/-) mice developed similar lung diseases. Dectin-1 deficiency decreased the infiltration of neutrophils and monocyte-derived macrophages and repressed the expansion of lung CD4(+)IL-17A(+) cells. The production of IL-23 p19 was reduced in Dectin-1(-/-) BMDCs.

conclusionsThese data suggested Dectin-1 plays a critical role in the development of fungus-induced HP.

Indexed as

TrichosporonAlveolitis, Extrinsic AllergicAnimalsBronchoalveolar Lavage FluidCell CountDectin-1Interleukin-23Lectins, C-TypeLungMice, Inbred C57BLMice, KnockoutTh17 CellsDectin-1dectin-2, mouseInterleukin-23Lectins, C-TypeDectin-1Hypersensitivity pneumonitisTh17Trichosporon asahii

Identifiers

PMID26644324
OpenAlexW2276245331

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.