Evidence map›Paper›PMID 28921377›Full record

ArticleJournal of gastroenterology2018

Basophils activated via TLR signaling may contribute to pathophysiology of type 1 autoimmune pancreatitis.

Masato Yanagawa, Kazushige Uchida, Yugo Ando, Takashi Tomiyama, Takashi Yamaguchi, Tsukasa Ikeura, Toshiro Fukui, Akiyoshi Nishio, Yoshiko Uemura, Takayuki Miyara and 3 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Journal of gastroenterology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  9. IgG4-related diseases of the digestive tract.Nature reviews. Gastroenterology & hepatology · 2022
    Review
  10. Review
  11. Review
  12. Review
  13. Article
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  15. Chronic Pancreatitis and the Development of Pancreatic Cancer.Endocrine, metabolic & immune disorders drug targets · 2020
    Review
  16. Immunological mechanism of IgG4-related disease.Journal of translational autoimmunity · 2020
    Article
  17. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 1 institution in 1 country.

Masato YanagawaThe Third Department of Internal Medicine, Division of Gastroenterology and Hepatology, Kansai Medical University, 2-5-1 Shinmachi, Hirakata, Osaka, 573-1010, Japan.
Kazushige UchidaThe Third Department of Internal Medicine, Division of Gastroenterology and Hepatology, Kansai Medical University, 2-5-1 Shinmachi, Hirakata, Osaka, 573-1010, Japan.
Yugo AndoThe Third Department of Internal Medicine, Division of Gastroenterology and Hepatology, Kansai Medical University, 2-5-1 Shinmachi, Hirakata, Osaka, 573-1010, Japan.
Takashi TomiyamaThe Third Department of Internal Medicine, Division of Gastroenterology and Hepatology, Kansai Medical University, 2-5-1 Shinmachi, Hirakata, Osaka, 573-1010, Japan.
Takashi YamaguchiThe Third Department of Internal Medicine, Division of Gastroenterology and Hepatology, Kansai Medical University, 2-5-1 Shinmachi, Hirakata, Osaka, 573-1010, Japan.
Tsukasa IkeuraThe Third Department of Internal Medicine, Division of Gastroenterology and Hepatology, Kansai Medical University, 2-5-1 Shinmachi, Hirakata, Osaka, 573-1010, Japan.
Toshiro FukuiThe Third Department of Internal Medicine, Division of Gastroenterology and Hepatology, Kansai Medical University, 2-5-1 Shinmachi, Hirakata, Osaka, 573-1010, Japan.
Akiyoshi NishioThe Third Department of Internal Medicine, Division of Gastroenterology and Hepatology, Kansai Medical University, 2-5-1 Shinmachi, Hirakata, Osaka, 573-1010, Japan.
Yoshiko UemuraDepartment of Pathology, Kansai Medical University, Hirakata, Japan.
Takayuki MiyaraThe First Department of Internal Medicine, Division of Hematology, Respiratory Medicine and Rheumatology, Kansai Medical University, Hirakata, Japan.
Hiroyuki OkamotoDepartment of Dermatology, Kansai Medical University, Hirakata, Japan.
Souhei SatoiDepartment of Surgery, Kansai Medical University, Hirakata, Japan.
Kazuichi OkazakiThe Third Department of Internal Medicine, Division of Gastroenterology and Hepatology, Kansai Medical University, 2-5-1 Shinmachi, Hirakata, Osaka, 573-1010, Japan. okazaki@hirakata.kmu.ac.jp.
Kansai Medical University · JP

Funding

Grant-in-Aid for Scientific Research (C) of the Ministry of Culture and Science of Japan 15K09052Grant-in-Aid for Scientific Research (C) of the Ministry of Culture and Science of Japan 26461038
6 · The paper itself

Abstract

backgroundPathophysiology of type 1 autoimmune pancreatitis (AIP) is still unclear. We previously reported that M2 macrophages might play an important role in type 1 AIP. Recently, it has been reported that basophils regulate differentiation to M2 macrophages. In this study, we investigated basophils from the pancreatic tissue and peripheral blood of individuals with type 1 AIP.

methodsBy using immunohistochemistry, we investigated basophils in pancreatic tissue from 13 patients with type 1 AIP and examined expression of toll-like receptors (TLRs) by these cells. Additionally, we obtained peripheral blood samples from 27 healthy subjects, 40 patients with type 1 AIP, 8 patients with alcoholic chronic pancreatitis, 10 patients with bronchial asthma, and 10 patients with atopic dermatitis, and analyzed activation of basophils by stimulating them with ligands of TLR1-9. We also compared TLR expression in basophils from the tissue and blood samples.

resultsBasophils were detected in pancreatic tissues from 10 of 13 patients with type 1 AIP. Flow cytometric analysis revealed that the ratios of basophils activated by TLR4 stimulation in type 1 AIP (9.875 ± 1.148%) and atopic dermatitis (11.768 ± 1.899%) were significantly higher than those in healthy subjects (5.051 ± 0.730%; P < 0.05). Levels of basophils activated by TLR2 stimulation were higher in seven type 1 AIP cases. Furthermore, stimulation of TLR2 and/or TLR4, which were expressed by basophils in pancreas, activated basophils in peripheral blood.

conclusionsBasophils activated via TLR signaling may play an important role in the pathophysiology of type 1 AIP.

Indexed as

AdultAgedAged, 80 and overAutoimmune DiseasesBasophilsFemaleHospitals, UniversityHumansImmunoglobulin GJapanMaleMiddle AgedPancreatitisSignal TransductionToll-Like Receptor 2Toll-Like Receptor 4Immunoglobulin GTLR2 protein, humanTLR4 protein, humanToll-Like Receptor 2Toll-Like Receptor 4Autoimmune pancreatitisBasophilM2 macrophageTLR

Identifiers

PMID28921377
PMCPMC5847205
OpenAlexW2755779646

What OpenQuestion holds

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Registered trials

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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.