Evidence map›Paper›PMID 42747404›Full record

ArticleJournal of human immunity2026

High prevalence of autoantibodies neutralizing type I IFNs in Japanese patients with hepatitis C.

Maki Taniguchi, Chiaki Tao, Takaki Asano, Miyuki Tsumura, Ko Ko, Hiroko Kumada, Takanori Utsumi, Kosuke Noma, Fumiaki Sakura, Kosuke Ashihara and 11 more

Abstract read
In one paragraph

Article in Journal of human immunity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

21 authors.

Maki Taniguchi *Department of Pediatrics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.ORCID 0009-0005-4035-1360
Chiaki Tao *Department of Pediatrics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.ORCID 0009-0007-9676-8688
Takaki Asano *Department of Pediatrics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.ORCID 0000-0003-1424-2433
Miyuki TsumuraDepartment of Pediatrics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.ORCID 0000-0002-8272-9588
Ko KoGraduate School of Biomedical and Health Sciences, Hiroshima University , Hiroshima, Japan.ORCID 0000-0002-6961-2000
Hiroko KumadaDepartment of Pediatrics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.ORCID 0009-0006-2069-6553
Takanori UtsumiDepartment of Pediatrics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.ORCID 0009-0003-3600-4484
Kosuke NomaDepartment of Pediatrics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.ORCID 0009-0009-9415-9744
Fumiaki SakuraDepartment of Pediatrics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.ORCID 0009-0000-8672-8868
Kosuke AshiharaDepartment of Pediatrics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.ORCID 0009-0001-9891-8770
Moe TamauraDepartment of Pediatrics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.ORCID 0000-0002-2743-2474
Yoko MizoguchiDepartment of Pediatrics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.ORCID 0000-0003-3686-9915
Osamu OharaDepartment of Applied Genomics, Kazusa DNA Research Institute, Chiba, Japan.ORCID 0000-0002-3328-9571
Dusan BogunovicDepartment of Pediatrics, Columbia University Medical Center, NY, NY, USA.ORCID 0000-0002-9277-3232
Paul BastardLaboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM, Paris, France.ORCID 0000-0002-5926-8437
Jean-Laurent CasanovaLaboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM, Paris, France.ORCID 0000-0002-7782-4169
Junko TanakaGraduate School of Biomedical and Health Sciences, Hiroshima University , Hiroshima, Japan.ORCID 0000-0002-5669-4051
Masataka TsugeLiver Center, Hiroshima University Hospital , Hiroshima, Japan.ORCID 0000-0001-7591-8287
Kazuaki ChayamaHiroshima Institute of Life Sciences , Hiroshima, Japan.ORCID 0000-0002-5530-5341
Shiro OkaDepartment of Gastroenterology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.ORCID 0000-0002-1652-0743
Satoshi Okada *Department of Pediatrics, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.ORCID 0000-0002-4622-5657

Funding

Japan Agency for Medical Research and Development JP21fk0108436Japan Agency for Medical Research and Development JP22fk0108514Japan Agency for Medical Research and Development JP23fk0210122Japan Agency for Medical Research and Development JP256f0137011Japan Agency for Medical Research and Development JP25ek0109802Japan Society for the Promotion of Science 22H03041Japan Society for the Promotion of Science 22KK0113Japan Society for the Promotion of Science 25K19230Japan Society for the Promotion of Science JPJS00420230011Tsuchiya Memorial Medical Foundation
6 · The paper itself

Abstract

Autoantibodies neutralizing type I IFNs (AAN-I-IFNs) are being identified as major, common, and global determinants of a growing range of severe viral diseases. We examined whether persistent hepatitis C virus (HCV) infection, with or without IFN-α therapy, could induce AAN-I-IFNs. We tested 2,573 HCV patients aged 1-95 years (1,115 treated with IFN-α, 1,458 untreated) and 1,000 healthy controls. AAN-INF-α2 prevalence was significantly higher in hepatitis C patients (2.7%) than in healthy controls (0.7%) and was higher still in those treated with IFN-α (3.9%) than in untreated patients (1.9%) (P = 0.0053). A longitudinal study of 15 IFN-α-treated patients with AAN-IFN-α2 revealed that only one had AAN-IFN-α2 before IFN-α therapy and that 12 patients developed AAN-IFN-α2 in the year following treatment. However, 80% eventually became AAN-IFN-α2 negative. These findings suggest that chronic HCV infection, perhaps due to the chronic production of endogenous IFN-α, and exogenous IFN-α treatment promote the development of AAN-IFN-α2.

Identifiers

PMID42747404
PMCPMC13580663

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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.