Evidence map›Paper›PMID 32917979›Full record

ArticleCellular & molecular immunology2021

IL-17 sustains the plasma cell response via p38-mediated Bcl-xL RNA stability in lupus pathogenesis.

Kongyang Ma, Wenhan Du, Fan Xiao, Man Han, Enyu Huang, Na Peng, Yuan Tang, Chong Deng, Lixiong Liu, Yulan Chen and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

34 citing papers in PubMed, 57 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 5 institutions in 3 countries.

Kongyang MaDepartment of Pathology and Shenzhen Institute of Research and Innovation, The University of Hong Kong; Chongqing International Institute for Immunology, Hong Kong, China.ORCID http://orcid.org/0000-0002-9739-7686
Wenhan DuDepartment of Pathology and Shenzhen Institute of Research and Innovation, The University of Hong Kong; Chongqing International Institute for Immunology, Hong Kong, China.
Fan XiaoDepartment of Pathology and Shenzhen Institute of Research and Innovation, The University of Hong Kong; Chongqing International Institute for Immunology, Hong Kong, China.ORCID http://orcid.org/0000-0003-4540-452X
Man HanDivision of Rheumatology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Enyu HuangDepartment of Pathology and Shenzhen Institute of Research and Innovation, The University of Hong Kong; Chongqing International Institute for Immunology, Hong Kong, China.
Na PengDepartment of Rheumatology and Nephrology, the Second People's Hospital, China Three Gorges University, Yichang, China.
Yuan TangDepartment of Pathology and Shenzhen Institute of Research and Innovation, The University of Hong Kong; Chongqing International Institute for Immunology, Hong Kong, China.
Chong DengDepartment of Pathology and Shenzhen Institute of Research and Innovation, The University of Hong Kong; Chongqing International Institute for Immunology, Hong Kong, China.
Lixiong LiuDepartment of Rheumatology and Immunology, Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, China.
Yulan ChenDepartment of Rheumatology and Immunology, Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, China.
Jingjing LiDepartment of Rheumatology and Immunology, Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, China.
Shiwen YuanDepartment of Rheumatology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Qin HuangDepartment of Rheumatology and Immunology, Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, China.
Xiaoping HongDepartment of Rheumatology and Immunology, Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, China.
Dajun HuDepartment of Rheumatology and Nephrology, the Second People's Hospital, China Three Gorges University, Yichang, China.
Xiaoyan CaiDepartment of Rheumatology, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Quan JiangDivision of Rheumatology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Dongzhou LiuDepartment of Rheumatology and Immunology, Second Clinical Medical College of Jinan University, Shenzhen People's Hospital, Shenzhen, China.
Liwei LuDepartment of Pathology and Shenzhen Institute of Research and Innovation, The University of Hong Kong; Chongqing International Institute for Immunology, Hong Kong, China. liweilu@hku.hk.ORCID http://orcid.org/0000-0002-8634-0967
Jinan University · CNCity University of Hong Kong, Shenzhen Research Institute · CNChina Three Gorges University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNGuangzhou First People's Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81771761National Natural Science Foundation of China (National Science Foundation of China) 81901635National Natural Science Foundation of China (National Science Foundation of China) 91842304
6 · The paper itself

Abstract

Recent studies have demonstrated a central role for plasma cells in the development of autoimmune diseases, such as systemic lupus erythematosus (SLE). Currently, both the phenotypic features and functional regulation of autoreactive plasma cells during SLE pathogenesis remain largely unclear. In this study, we first found that a major subset of IL-17 receptor-expressing plasma cells potently produced anti-dsDNA IgG upon IL-17A (IL-17) stimulation in SLE patients and lupus mice. Using a humanized lupus mouse model, we showed that the transfer of Th17 cell-depleted PBMCs from lupus patients resulted in a significantly reduced plasma cell response and attenuated renal damage in recipient mice compared to the transfer of total SLE PBMCs. Moreover, long-term BrdU incorporation in lupus mice detected highly enriched long-lived BrdU

Indexed as

Lupus Erythematosus, SystemicPlasma CellsAnimalsGerminal CenterHumansInterleukin-17MiceRNA StabilityIl17a protein, mouseInterleukin-17AutoantibodyInterleukin-17A (IL-17)Plasma cell (PC)Systemic lupus erythematosus (SLE)

Identifiers

PMID32917979
PMCPMC8245411
OpenAlexW3086333576

What OpenQuestion holds

Textmetadata
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.