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Increased circulating innate lymphoid cell (ILC)1 and decreased circulating ILC3 are involved in the pathogenesis of Henoch-Schonlein purpura
BACKGROUND: Innate lymphoid cell (ILC) dysfunction is involved in numerous immune diseases, but this has not been demonstrated in Henoch-Schonlein purpura (HSP). This study aimed to investigate whether ILC dysfunction or imbalance participate in the pathogenesis of HSP. METHODS: This was a prospecti...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9003988/ https://www.ncbi.nlm.nih.gov/pubmed/35413831 http://dx.doi.org/10.1186/s12887-022-03262-w |
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author | Zhang, Lili Lin, Qiang Jiang, Lijun Wu, Mingfu Huang, Linlin Quan, Wei Li, Xiaozhong |
author_facet | Zhang, Lili Lin, Qiang Jiang, Lijun Wu, Mingfu Huang, Linlin Quan, Wei Li, Xiaozhong |
author_sort | Zhang, Lili |
collection | PubMed |
description | BACKGROUND: Innate lymphoid cell (ILC) dysfunction is involved in numerous immune diseases, but this has not been demonstrated in Henoch-Schonlein purpura (HSP). This study aimed to investigate whether ILC dysfunction or imbalance participate in the pathogenesis of HSP. METHODS: This was a prospective study in patients with HSP who were hospitalized at the Children’s Hospital of Soochow University from June to December 2019. Age- and sex-matched controls were also enrolled. ILC subsets and lymphocyte subpopulations were determined by flow cytometry. The transmission immune turbidimetric method also facilitated the exploration of correlations between ILC subset frequency and lymphocyte subpopulation, as well as serum IgA in HSP patients. RESULTS: Fifty-one patients with HSP and 22 control patients were included. There were no differences in age and sex between the two groups. Compared with controls, patients with HSP had higher ILCs in relation to lymphocytes (P = 0.036), higher ILCs in relation to PBMCs (P = 0.026), higher ILC1s (P < 0.001), lower ILC3s (P < 0.05), and higher ILC1/ILC3 ratio (P < 0.001). Sixteen patients underwent routine therapy combined with methylprednisolone for 7–10 days; ILC1s were significantly decreased (P < 0.001) and ILC3s were increased (P = 0.033), and ILC1/ILC3 was significantly decreased (P < 0.001). Compared with the controls, the ratios of ILCs/lymphocytes and ILCs/PBMC were higher in patients in the arthritis and mixed groups (all P < 0.05). ILC1 were elevated in the purpura, arthritis, abdominal, and mixed groups (P = 0.027, P = 0.007, P < 0.001, and P < 0.001, respectively). ILC1/ILCs were positively correlated with CD3 + CD8 + T lymphocytes (r = 0.3701, P = 0.0075). The level of IgA did not correlate with ILCs. CONCLUSIONS: Higher circulating ILC1s and lower circulating ILC3s appear to be involved in the pathogenesis of HSP. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12887-022-03262-w. |
format | Online Article Text |
id | pubmed-9003988 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-90039882022-04-13 Increased circulating innate lymphoid cell (ILC)1 and decreased circulating ILC3 are involved in the pathogenesis of Henoch-Schonlein purpura Zhang, Lili Lin, Qiang Jiang, Lijun Wu, Mingfu Huang, Linlin Quan, Wei Li, Xiaozhong BMC Pediatr Research BACKGROUND: Innate lymphoid cell (ILC) dysfunction is involved in numerous immune diseases, but this has not been demonstrated in Henoch-Schonlein purpura (HSP). This study aimed to investigate whether ILC dysfunction or imbalance participate in the pathogenesis of HSP. METHODS: This was a prospective study in patients with HSP who were hospitalized at the Children’s Hospital of Soochow University from June to December 2019. Age- and sex-matched controls were also enrolled. ILC subsets and lymphocyte subpopulations were determined by flow cytometry. The transmission immune turbidimetric method also facilitated the exploration of correlations between ILC subset frequency and lymphocyte subpopulation, as well as serum IgA in HSP patients. RESULTS: Fifty-one patients with HSP and 22 control patients were included. There were no differences in age and sex between the two groups. Compared with controls, patients with HSP had higher ILCs in relation to lymphocytes (P = 0.036), higher ILCs in relation to PBMCs (P = 0.026), higher ILC1s (P < 0.001), lower ILC3s (P < 0.05), and higher ILC1/ILC3 ratio (P < 0.001). Sixteen patients underwent routine therapy combined with methylprednisolone for 7–10 days; ILC1s were significantly decreased (P < 0.001) and ILC3s were increased (P = 0.033), and ILC1/ILC3 was significantly decreased (P < 0.001). Compared with the controls, the ratios of ILCs/lymphocytes and ILCs/PBMC were higher in patients in the arthritis and mixed groups (all P < 0.05). ILC1 were elevated in the purpura, arthritis, abdominal, and mixed groups (P = 0.027, P = 0.007, P < 0.001, and P < 0.001, respectively). ILC1/ILCs were positively correlated with CD3 + CD8 + T lymphocytes (r = 0.3701, P = 0.0075). The level of IgA did not correlate with ILCs. CONCLUSIONS: Higher circulating ILC1s and lower circulating ILC3s appear to be involved in the pathogenesis of HSP. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12887-022-03262-w. BioMed Central 2022-04-12 /pmc/articles/PMC9003988/ /pubmed/35413831 http://dx.doi.org/10.1186/s12887-022-03262-w Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Zhang, Lili Lin, Qiang Jiang, Lijun Wu, Mingfu Huang, Linlin Quan, Wei Li, Xiaozhong Increased circulating innate lymphoid cell (ILC)1 and decreased circulating ILC3 are involved in the pathogenesis of Henoch-Schonlein purpura |
title | Increased circulating innate lymphoid cell (ILC)1 and decreased circulating ILC3 are involved in the pathogenesis of Henoch-Schonlein purpura |
title_full | Increased circulating innate lymphoid cell (ILC)1 and decreased circulating ILC3 are involved in the pathogenesis of Henoch-Schonlein purpura |
title_fullStr | Increased circulating innate lymphoid cell (ILC)1 and decreased circulating ILC3 are involved in the pathogenesis of Henoch-Schonlein purpura |
title_full_unstemmed | Increased circulating innate lymphoid cell (ILC)1 and decreased circulating ILC3 are involved in the pathogenesis of Henoch-Schonlein purpura |
title_short | Increased circulating innate lymphoid cell (ILC)1 and decreased circulating ILC3 are involved in the pathogenesis of Henoch-Schonlein purpura |
title_sort | increased circulating innate lymphoid cell (ilc)1 and decreased circulating ilc3 are involved in the pathogenesis of henoch-schonlein purpura |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9003988/ https://www.ncbi.nlm.nih.gov/pubmed/35413831 http://dx.doi.org/10.1186/s12887-022-03262-w |
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