Evidence map›Paper›PMID 25973893›Full record

ArticlePloS one2015

Decreased Expression of Innate Immunity-Related Genes in Peripheral Blood Mononuclear Cells from Patients with IgG4-Related Disease.

Akio Nakajima, Yasufumi Masaki, Takuji Nakamura, Takafumi Kawanami, Yasuhito Ishigaki, Tsutomu Takegami, Mitsuhiro Kawano, Kazunori Yamada, Norifumi Tsukamoto, Shoko Matsui and 22 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. 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
1.3field-weighted citation impact, top 21% 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, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Omics in IgG4-related disease.Chinese medical journal · 2025
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  13. Observational
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

32 authors at 15 institutions in 1 country.

Akio NakajimaHematology and Immunology, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, Japan.
Yasufumi MasakiHematology and Immunology, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, Japan.
Takuji NakamuraHematology and Immunology, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, Japan.
Takafumi KawanamiHematology and Immunology, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, Japan.
Yasuhito IshigakiMedical Research Institute, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, Japan.
Tsutomu TakegamiMedical Research Institute, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, Japan.
Mitsuhiro KawanoDivision of Rheumatology, Department of Internal Medicine, Kanazawa University Hospital, Ishikawa 920-8641, Japan.
Kazunori YamadaDivision of Rheumatology, Department of Internal Medicine, Kanazawa University Hospital, Ishikawa 920-8641, Japan.
Norifumi TsukamotoDepartment of Medicine and Clinical Science, Gunma University Graduate School of Medicine, Gunma 371-8511, Japan.
Shoko MatsuiHealth Administration Center University of Toyama, Toyama 930-0194, Japan.
Takako SaekiDepartment of Internal Medicine, Nagaoka Red Cross Hospital, Niigata 940-2085, Japan.
Kazuichi OkazakiThird Department of Internal Medicine, Division of Gastroenterology and Hepatology, Kansai Medical University, Osaka 573-1191, Japan.
Terumi KamisawaDepartment of Internal Medicine, Tokyo Metropolitan Komagome Hospital, Tokyo 113-8677, Japan.
Taiichiro MiyashitaDepartment of Rheumatology, National Hospital Organization Nagasaki Medical center, Nagasaki 380-8582, Japan.
Yoshihiro YakushijinDepartment of Clinical Oncology, Ehime Graduate School of Medicine, Ehime 791-0295, Japan.
Keita FujikawaDepartment of Rheumatology, Japan Community Healthcare Organization, Isahaya General Hospital, Nagasaki 854-8501, Japan.
Motohisa YamamotoDepartment of Gastroenterology, Rheumatology and Clinical Immunology, Sapporo Medical University School of Medicine, Hokkaido 060-8543, Japan.
Hideaki HamanoMedical Informatics Division and Department of Internal Medicine, Gastroenterology, Shinshu University School Hospital, Nagano 390-8621, Japan.
Tomoki OriguchiFirst Department of Internal Medicine, Department of Immunology and Rheumatology, Nagasaki Graduate School of Health Sciences, Nagasaki 852-8520, Japan.
Shintaro HirataFirst Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, Fukuoka 807-8555, Japan.
Hiroto TsuboiDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Takayuki SumidaDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan.
Hisanori MorimotoDivision of Nephrology, Mitoyo General Hospital, Kagawa 769-1695, Japan.
Tomomi SatoHematology and Immunology, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, Japan.
Haruka IwaoHematology and Immunology, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, Japan.
Miyuki MikiHematology and Immunology, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, Japan.
Tomoyuki SakaiHematology and Immunology, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, Japan.
Yoshimasa FujitaHematology and Immunology, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, Japan.
Masao TanakaHematology and Immunology, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, Japan.
Toshihiro FukushimaHematology and Immunology, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, Japan.
Toshiro OkazakiHematology and Immunology, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, Japan.
Hisanori UmeharaHematology and Immunology, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, Japan; Department of Clinical Immunology, Graduate School of Medicine and Faculty of Medicine, Kyoto University, Kyoto 606-8501, Japan.
Kanazawa Medical University · JPKanazawa University Hospital · JPUniversity of Tsukuba · JPEhime University · JPGunma University · JPJapan Community Healthcare Organization · JPKansai Medical University · JPMito Saiseikai General Hospital · JPNagaoka Red Cross Hospital · JPNagasaki Medical Center · JPSapporo Medical University · JPShinshu University · JPTokyo Metropolitan Komagome Hospital · JPUniversity of Occupational and Environmental Health Japan · JPUniversity of Toyama · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIgG4-related disease (IgG4-RD) is a new clinical entity of unknown etiology characterized by elevated serum IgG4 and tissue infiltration by IgG4-positive plasma cells. Although aberrancies in acquired immune system functions, including increases in Th2 and Treg cytokines observed in patients with IgG4-RD, its true etiology remains unclear. To investigate the pathogenesis of IgG4-RD, this study compared the expression of genes related to innate immunity in patients with IgG4-RD and healthy controls. MATERIALS AND

methodsPeripheral blood mononuclear cells (PBMCs) were obtained from patients with IgG4-RD before and after steroid therapy and from healthy controls. Total RNA was extracted and DNA microarray analysis was performed in two IgG4-RD patients to screen for genes showing changes in expression. Candidate genes were validated by real-time RT-PCR in 27 patients with IgG4-RD and 13 healthy controls.

resultsDNA microarray analysis identified 21 genes that showed a greater than 3-fold difference in expression between IgG4-RD patients and healthy controls and 30 genes that showed a greater than 3-fold change in IgG4-RD patients following steroid therapy. Candidate genes related to innate immunity, including those encoding Charcot-Leyden crystal protein (CLC), membrane-spanning 4-domain subfamily A member 3 (MS4A3), defensin alpha (DEFA) 3 and 4, and interleukin-8 receptors (IL8R), were validated by real-time RT-PCR. Expression of all genes was significantly lower in IgG4-RD patients than in healthy controls. Steroid therapy significantly increased the expression of DEFA3, DEFA4 and MS4A3, but had no effect on the expression of CLC, IL8RA and IL8RB.

conclusionsThe expression of genes related to allergy or innate immunity, including CLC, MS4A3, DEFA3, DEFA4, IL8RA and IL8RB, was lower in PBMCs from patients with IgG4-RD than from healthy controls. Although there is the limitation in the number of patients applied in DNA microarray, impaired expression of genes related to innate immunity may be involved in the pathogenesis of IgG4-RD as well as in abnormalities of acquired immunity.

Indexed as

AdultAgedAged, 80 and overalpha-DefensinsAutoimmune DiseasesCase-Control StudiesCell Cycle ProteinsDown-RegulationFemaleGlycoproteinsHumansImmunity, InnateImmunoglobulin GLeukocytes, MononuclearLysophospholipaseMalealpha-DefensinsCell Cycle ProteinsGlycoproteinshuman neutrophil peptide 3human neutrophil peptide 4Immunoglobulin Glysolecithin acylhydrolaseLysophospholipaseMembrane ProteinsMS4A3 protein, humanReceptors, Interleukin-8

Identifiers

PMID25973893
PMCPMC4431830
OpenAlexW921856682

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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.