Evidence map›Paper›PMID 42565578›Full record

ReviewZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences2026

[Role of HLA genetic variants in autoimmune diseases].

Tai Rao, Lulu Chen, Qianhe Wei, Dongsheng Ouyang

Abstract readReviewEnglish Abstract
In one paragraph

Review in Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

4 authors.

Tai RaoDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008. raotai9298@csu.edu.cn.
Lulu ChenHunan Key Laboratory for Bioanalysis of Complex Matrix Samples, Changsha Duxact Biotech Co., Ltd., Changsha 410205.
Qianhe WeiHunan Key Laboratory for Bioanalysis of Complex Matrix Samples, Changsha Duxact Biotech Co., Ltd., Changsha 410205.
Dongsheng OuyangDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008. ouyangyj@163.com.

Funding

the Changsha Major Science and Technology Projects China. kh2401014the Natural Science Foundation of Hunan Province (), and the Changsha Major Science and Technology Projects (kh2401014), China. 2026JJ50638This work was supported by the National Natural Science Foundation 82274032
6 · The paper itself

Abstract

Autoimmune diseases are a group of disorders caused by dysregulated immune function, in which the immune system mistakenly attacks the host's own healthy cells, tissues, and organs. Genetic factors are one of the important foundations for the development of autoimmune diseases. Human leukocyte antigen (HLA) is closely related to immune function in the human body, and HLA-encoding genes are highly polymorphic, making them important susceptibility factors for autoimmune diseases. HLA genetic variants are closely associated with a variety of autoimmune diseases, and they mediate the occurrence and development of these diseases through multiple mechanisms, such as molecular mimicry and self-antigen presentation. They have also been importantly applied in clinical disease prevention, diagnosis, and treatment. An in-depth understanding of the relationship between HLA genetic variants and autoimmune diseases is of great significance for discovering biomarkers related to disease prevention, diagnosis, treatment, and prognosis, elucidating disease pathogenesis, and developing new therapeutic strategies. However, substantial challenges remain in the basic research and clinical translation of autoimmune disease-associated HLA variants. Multi-omics technologies have important application prospects and significance in the field of HLA-related autoimmune diseases and may provide new directions for mechanistic research and clinical application of HLA genetic variants in autoimmune diseases.

Indexed as

Autoimmune DiseasesGenetic VariationHLA AntigensGenetic Predisposition to DiseaseHumansPolymorphism, GeneticHLA Antigensautoimmune diseasesclinical applicationgenetic variationhuman leukocyte antigenmechanism of actionmulti-omics

Identifiers

PMID42565578
PMCPMC13407289

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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.