Evidence map›Paper›PMID 40770293›Full record

ArticleBMC nephrology2025

Immunomodulatory effect of CD71

Batool Zamani, Fatemeh Riazian, Masoud Moeini Taba, Afshin Namdar, Fateme Zareei Barzoki, Abdolamir Atapour, Hossein Motedayyen

Abstract read
In one paragraph

Article in BMC nephrology, 2025. 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

7 authors.

Batool ZamaniAutoimmune Diseases Research Center, Kashan University of Medical Sciences, Kashan, Iran.
Fatemeh RiazianDepartment of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran.
Masoud Moeini TabaDepartment of Internal Medicine, School of Medicine, Kashan University of Medical Sciences, Kashan, Iran.
Afshin NamdarPeter Gilgan Centre for Research and Learning, The Hospital for Sick Children (SickKids), Toronto, ON, CA, Canada.
Fateme Zareei BarzokiAutoimmune Diseases Research Center, Kashan University of Medical Sciences, Kashan, Iran.
Abdolamir AtapourIsfahan Kidney Diseases Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.
Hossein MotedayyenAutoimmune Diseases Research Center, Kashan University of Medical Sciences, Kashan, Iran. hmotedayyen@gmail.com.

Funding

kashan university 99255
6 · The paper itself

Abstract

backgroundImmune abnormalities play a critical role in the pathogenesis of kidney failure. CD71

methodsPBMCs were isolated from 49 kidney failure patients and 20 healthy subjects. The frequencies of T cell subsets and CD71 + erythroid cells were determined by flow cytometry. The numbers of reticulocytes and RBCs were also measured. Panel-reactive antibodies screening was used to assess antibodies against human leukocyte antigens (HLAs) in the patients. The effect of CD71 + erythroid cells on PBMC proliferation in kidney failure patients was investigated using a CFSE labeling assay. Erythropoietin level was measured by ELISA.

resultsKidney failure patients showed a significant increase in CD71 + erythroid cells (P < 0.01). In contrast, the frequencies of Th1, Th2, and Th17 cells were significantly reduced in these patients (P < 0.01-0.05). Among CD4 + T subsets, Th1 cell frequency was inversely correlated with the number of CD71 + erythroid cells (P < 0.05). In vitro, CD71 + erythroid cells inhibited the proliferation of PMBCs in kidney failure patients (P < 0.0001-0.05). No significant difference was observed in Treg frequencies between patients and controls. The frequency of CD71 + erythroid cells was significantly decreased in kidney failure patients with anti-HLA antibodies, unlike patients without anti-HLA antibodies (P < 0.001). The patients had an increased number of reticulocytes, unlike RBC, in peripheral blood compared with healthy subjects (P < 0.01-0.05). The patients exhibited a reduction in erythropoietin level compared with the control group (P < 0.0001).

conclusionThese findings suggest CD71 + erythroid cells may contribute to immune dysregulation in kidney failure patients, potentially playing a role in disease progression and its immunopathology.

Indexed as

Antigens, CDErythroid CellsReceptors, TransferrinRenal InsufficiencyAdultAgedCell ProliferationErythropoietinFemaleHumansLeukocytes, MononuclearMaleMiddle AgedT-Lymphocytes, RegulatoryAntigens, CDCD71 antigenErythropoietinReceptors, TransferrinCD71 + erythroid cellsImmunomodulatory effectsKidney failureRegulatory T cells

Identifiers

PMID40770293
PMCPMC12329980

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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.