Evidence map›Paper›PMID 28680376›Full record

ReviewImmune network2017

Dendritic Cell Dysfunction in Patients with End-stage Renal Disease.

Ji Ung Kim, Miyeon Kim, Sinae Kim, Tam Thanh Nguyen, Eunhye Kim, Siyoung Lee, Soohyun Kim, Hyunwoo Kim

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Immune network, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.2field-weighted citation impact, top 12% 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, 42 citations in OpenAlex.

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  13. Humoral response to BNT162b2 mRNA COVID-19 vaccine in peritoneal and hemodialysis patients: A comparative study.Therapeutic apheresis and dialysis : official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy · 2022
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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

8 authors at 2 institutions in 1 country.

Ji Ung KimDivision of Nephrology, Department of Internal Medicine, Jeju National University Hospital, Jeju National University School of Medicine, Jeju 63241, Korea.
Miyeon KimDivision of Nephrology, Department of Internal Medicine, Jeju National University Hospital, Jeju National University School of Medicine, Jeju 63241, Korea.
Sinae KimLaboratory of Cytokine Immunology, Department of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea.
Tam Thanh NguyenLaboratory of Cytokine Immunology, Department of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea.
Eunhye KimLaboratory of Cytokine Immunology, Department of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea.
Siyoung LeeLaboratory of Cytokine Immunology, Department of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea.
Soohyun KimLaboratory of Cytokine Immunology, Department of Biomedical Science and Technology, Konkuk University, Seoul 05029, Korea.
Hyunwoo KimDivision of Nephrology, Department of Internal Medicine, Jeju National University Hospital, Jeju National University School of Medicine, Jeju 63241, Korea.
Konkuk University · KRAdbiotech (South Korea) · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

End-stage renal disease (ESRD) with immune disorder involves complex interactions between the innate and adaptive immune responses. ESRD is associated with various alterations in immune function such as a reduction in polymorphonuclear leukocyte bactericidal activity, a suppression of lymphocyte proliferative response to stimuli, and a malfunction of cell-mediated immunity at the molecular level. ESRD also increases patients' propensity for infections and malignancies as well as causing a diminished response to vaccination. Several factors influence the immunodeficiency in patients with ESRD, including uremic toxins, malnutrition, chronic inflammation, and the therapeutic dialysis modality. The alteration of T-cell function in ESRD has been considered to be a major factor underlying the impaired adaptive cellular immunity in these patients. However, cumulative evidence has suggested that the immune defect in ESRD can be caused by an Ag-presenting dendritic cell (DC) dysfunction in addition to a T-cell defect. It has been reported that ESRD has a deleterious effect on DCs both in terms of their number and function, although the precise mechanism by which DC function becomes altered in these patients is unclear. In this review, we discuss the effects of ESRD on the number and function of DCs and propose a possible molecular mechanism for DC dysfunction. We also address therapeutic approaches to improve immune function by optimally activating DCs in patients with ESRD.

Indexed as

Antigen presenting cellsCostimulatory moleculeDendritic cellsEnd-stage renal diseaseImmunodeficiency

Identifiers

PMID28680376
PMCPMC5484645
OpenAlexW2628611714

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.