Evidence map›Paper›PMID 32180373›Full record

ArticleImmunity, inflammation and disease2020

Excessive ADAM17 activation occurs in uremic patients and may contribute to their immunocompromised status.

Mitsuru Yashiro, Masaki Ohya, Toru Mima, Yuri Nakashima, Kazuki Kawakami, Tomohiro Sonou, Koichi Tatsuta, Yukiko Yamano, Shigeo Negi, Takashi Shigematsu

Open access · goldAbstract read
In one paragraph

Article in Immunity, inflammation and disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 42% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Mitsuru YashiroDepartment of Nephrology, Wakayama Medical University, Wakayama, Japan.ORCID 0000-0002-6147-9153
Masaki OhyaDepartment of Nephrology, Wakayama Medical University, Wakayama, Japan.
Toru MimaDepartment of Nephrology, Wakayama Medical University, Wakayama, Japan.
Yuri NakashimaDepartment of Nephrology, Wakayama Medical University, Wakayama, Japan.
Kazuki KawakamiDepartment of Nephrology, Wakayama Medical University, Wakayama, Japan.
Tomohiro SonouDepartment of Nephrology, Wakayama Medical University, Wakayama, Japan.
Koichi TatsutaDepartment of Nephrology, Wakayama Medical University, Wakayama, Japan.
Yukiko YamanoDepartment of Nephrology, Wakayama Medical University, Wakayama, Japan.
Shigeo NegiDepartment of Nephrology, Wakayama Medical University, Wakayama, Japan.
Takashi ShigematsuDepartment of Nephrology, Wakayama Medical University, Wakayama, Japan.
Wakayama Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionWe previously reported that fibroblast growth factor 23 (FGF23)-klotho signaling plays a role in B cell immunity. Despite high serum levels of FGF23, a decline in immunity is frequently observed in patients on hemodialysis (HD); thus, abnormalities in the FGF23-klotho signaling pathway in immune cells may occur in these patients.

methodsWe analyzed the number of klotho-positive cells in peripheral blood mononuclear cells from 10 male and 6 female patients on HD and 5 healthy male subjects using flow cytometry. We analyzed the abundance of cleaved klotho protein in the murine B cell line, A20, and in the serum of HD patients and healthy subjects (HS) using flow cytometry and Western blotting. The serum level of A disintegrin and metalloprotease 17 (ADAM17) was measured in HD patients and HS using enzyme-linked immunosorbent assay.

resultsThe number of klotho-positive B cells was reduced in HD patients. Serum ADAM17 was responsible for the reduction in klotho, as a specific ADAM17 inhibitor reversed this change. The total serum levels of ADAM17 were similar in HD patients and HS; however, activated ADAM17 was increased in the serum of HD patients.

conclusionsWe concluded that abnormal ADAM17 activation could contribute to the immunocompromised status in patients on HD, in line with the reported role of ADAM17 as an anti-inflammatory and immunosuppressive factor.

Indexed as

ADAM17 ProteinAgedAged, 80 and overAnimalsCase-Control StudiesCell LineFemaleFibroblast Growth Factor-23Fibroblast Growth FactorsGlucuronidaseHumansImmunocompromised HostKlotho ProteinsLeukocytes, MononuclearMaleMiceADAM17 ProteinADAM17 protein, humanFGF23 protein, humanFgf23 protein, mouseFibroblast Growth Factor-23Fibroblast Growth FactorsGlucuronidaseKlotho ProteinsCKDklothoTACE

Identifiers

PMID32180373
PMCPMC7212198
OpenAlexW3011622737

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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.