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Increased circulating Tfh to Tfr ratio in chronic renal allograft dysfunction: a pilot study
BACKGROUND: T follicular helper (Tfh) cells play a control role in contribution of B cell differentiation and antibody production. T follicular regulatory (Tfr) cells inhibit Tfh-B cell interaction. METHODS: To identify whether circulating Tfh (cTfh) and Tfr (cTfr) cells contribute to chronic renal...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6683539/ https://www.ncbi.nlm.nih.gov/pubmed/31382877 http://dx.doi.org/10.1186/s12865-019-0308-x |
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author | Yan, Lin Li, Yamei Li, Yi Wu, Xiaojuan Wang, Xianding Wang, Lanlan Shi, Yunying Tang, Jiangtao |
author_facet | Yan, Lin Li, Yamei Li, Yi Wu, Xiaojuan Wang, Xianding Wang, Lanlan Shi, Yunying Tang, Jiangtao |
author_sort | Yan, Lin |
collection | PubMed |
description | BACKGROUND: T follicular helper (Tfh) cells play a control role in contribution of B cell differentiation and antibody production. T follicular regulatory (Tfr) cells inhibit Tfh-B cell interaction. METHODS: To identify whether circulating Tfh (cTfh) and Tfr (cTfr) cells contribute to chronic renal allograft dysfunction (CAD), 67 kidney transplant recipients (34 recipients with CAD, 33 recipients with stable function) were enrolled. The frequency of cTfh and cTfr cells, the level of serum CXCL13 were measured. RESULTS: The frequency of cTfr cells in CAD group was significantly lower than that in stable group (0.31% vs 0.68%, P = 0.002). The cTfh to cTfr ratio in CAD group was significantly higher than that in stable group (55.4 vs 25.3, P = 0.013). Serum CXCL13 in CAD group was significantly higher than stable group (30.4 vs 21.9 ng/ml, P = 0.025). After linear regression analysis, the cTfh to cTfr ratio was an independent risk factor for estimated glomerular filtration rate (eGFR) in recipients (standardized coefficient = − 0.420, P = 0.012). After logistic regression analysis, the cTfh to cTfr ratio was an independent risk factor for CAD (OR = 1.043, 95%CI = 1.004–1.085, P = 0.031). CONCLUSION: The imbalance between cTfh and cTfr cells contribute to the development of CAD. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12865-019-0308-x) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-6683539 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-66835392019-08-09 Increased circulating Tfh to Tfr ratio in chronic renal allograft dysfunction: a pilot study Yan, Lin Li, Yamei Li, Yi Wu, Xiaojuan Wang, Xianding Wang, Lanlan Shi, Yunying Tang, Jiangtao BMC Immunol Research Article BACKGROUND: T follicular helper (Tfh) cells play a control role in contribution of B cell differentiation and antibody production. T follicular regulatory (Tfr) cells inhibit Tfh-B cell interaction. METHODS: To identify whether circulating Tfh (cTfh) and Tfr (cTfr) cells contribute to chronic renal allograft dysfunction (CAD), 67 kidney transplant recipients (34 recipients with CAD, 33 recipients with stable function) were enrolled. The frequency of cTfh and cTfr cells, the level of serum CXCL13 were measured. RESULTS: The frequency of cTfr cells in CAD group was significantly lower than that in stable group (0.31% vs 0.68%, P = 0.002). The cTfh to cTfr ratio in CAD group was significantly higher than that in stable group (55.4 vs 25.3, P = 0.013). Serum CXCL13 in CAD group was significantly higher than stable group (30.4 vs 21.9 ng/ml, P = 0.025). After linear regression analysis, the cTfh to cTfr ratio was an independent risk factor for estimated glomerular filtration rate (eGFR) in recipients (standardized coefficient = − 0.420, P = 0.012). After logistic regression analysis, the cTfh to cTfr ratio was an independent risk factor for CAD (OR = 1.043, 95%CI = 1.004–1.085, P = 0.031). CONCLUSION: The imbalance between cTfh and cTfr cells contribute to the development of CAD. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12865-019-0308-x) contains supplementary material, which is available to authorized users. BioMed Central 2019-08-05 /pmc/articles/PMC6683539/ /pubmed/31382877 http://dx.doi.org/10.1186/s12865-019-0308-x Text en © The Author(s). 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Yan, Lin Li, Yamei Li, Yi Wu, Xiaojuan Wang, Xianding Wang, Lanlan Shi, Yunying Tang, Jiangtao Increased circulating Tfh to Tfr ratio in chronic renal allograft dysfunction: a pilot study |
title | Increased circulating Tfh to Tfr ratio in chronic renal allograft dysfunction: a pilot study |
title_full | Increased circulating Tfh to Tfr ratio in chronic renal allograft dysfunction: a pilot study |
title_fullStr | Increased circulating Tfh to Tfr ratio in chronic renal allograft dysfunction: a pilot study |
title_full_unstemmed | Increased circulating Tfh to Tfr ratio in chronic renal allograft dysfunction: a pilot study |
title_short | Increased circulating Tfh to Tfr ratio in chronic renal allograft dysfunction: a pilot study |
title_sort | increased circulating tfh to tfr ratio in chronic renal allograft dysfunction: a pilot study |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6683539/ https://www.ncbi.nlm.nih.gov/pubmed/31382877 http://dx.doi.org/10.1186/s12865-019-0308-x |
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