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T lymphocyte subset imbalances in patients contribute to ankylosing spondylitis
Ankylosing spondylitis is a chronic inflammatory rheumatic disease, which is characterized by inflammation of the spine and the sacroiliac joints. To date, the disease etiology remains unclear. In the present study, the correlation of T lymphocyte subset changes with the progression of ankylosing sp...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4247318/ https://www.ncbi.nlm.nih.gov/pubmed/25452811 http://dx.doi.org/10.3892/etm.2014.2046 |
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author | WANG, CHENGGONG LIAO, QIANDE HU, YIHE ZHONG, DA |
author_facet | WANG, CHENGGONG LIAO, QIANDE HU, YIHE ZHONG, DA |
author_sort | WANG, CHENGGONG |
collection | PubMed |
description | Ankylosing spondylitis is a chronic inflammatory rheumatic disease, which is characterized by inflammation of the spine and the sacroiliac joints. To date, the disease etiology remains unclear. In the present study, the correlation of T lymphocyte subset changes with the progression of ankylosing spondylitis was investigated. A total of 55 patients with ankylosing spondylitis (22 severe and 23 mild cases) and 20 healthy individuals were selected. Firstly, the punctured cells in the lesions and the serum were collected, and the lymphocytes and the peripheral blood mononuclear cells were prepared. Secondly, quantitative PCR, ELISA and flow cytometry analyses were carried out to detect the levels of a series of immunoglobulins, complements, helper T cells, cytotoxic T cells, regulatory cells and cytokines. The expression levels of α-globulin, γ-globulin, immunoglobulin (Ig)G, IgA, IgM, serum complement C3, and complement C4 were found to be significantly increased in ankylosing spondylitis patients. In addition, the percentage of Th1 and Th17 cells was found to be significantly higher in the ankylosing spondylitis groups (mild and severe) compared with the healthy individuals. As a result, the Th1/Th2 and Th17/Treg ratios were significantly higher in patients with ankylosing spondylitis. In addition, T lymphocyte subset ratio imbalances contributed to an increased expression of immune mediators, including interferon (IFN)-γ and interleukin (IL)-17A. The mRNA and protein expression levels of IFN-γ and IL-17A were found to be higher in the ankylosing spondylitis groups compared with the control group. The present study provided further evidence on the function and underlying mechanism of T lymphocyte subsets, which may be useful in the diagnosis and treatment of ankylosing spondylitis. |
format | Online Article Text |
id | pubmed-4247318 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-42473182014-12-01 T lymphocyte subset imbalances in patients contribute to ankylosing spondylitis WANG, CHENGGONG LIAO, QIANDE HU, YIHE ZHONG, DA Exp Ther Med Articles Ankylosing spondylitis is a chronic inflammatory rheumatic disease, which is characterized by inflammation of the spine and the sacroiliac joints. To date, the disease etiology remains unclear. In the present study, the correlation of T lymphocyte subset changes with the progression of ankylosing spondylitis was investigated. A total of 55 patients with ankylosing spondylitis (22 severe and 23 mild cases) and 20 healthy individuals were selected. Firstly, the punctured cells in the lesions and the serum were collected, and the lymphocytes and the peripheral blood mononuclear cells were prepared. Secondly, quantitative PCR, ELISA and flow cytometry analyses were carried out to detect the levels of a series of immunoglobulins, complements, helper T cells, cytotoxic T cells, regulatory cells and cytokines. The expression levels of α-globulin, γ-globulin, immunoglobulin (Ig)G, IgA, IgM, serum complement C3, and complement C4 were found to be significantly increased in ankylosing spondylitis patients. In addition, the percentage of Th1 and Th17 cells was found to be significantly higher in the ankylosing spondylitis groups (mild and severe) compared with the healthy individuals. As a result, the Th1/Th2 and Th17/Treg ratios were significantly higher in patients with ankylosing spondylitis. In addition, T lymphocyte subset ratio imbalances contributed to an increased expression of immune mediators, including interferon (IFN)-γ and interleukin (IL)-17A. The mRNA and protein expression levels of IFN-γ and IL-17A were found to be higher in the ankylosing spondylitis groups compared with the control group. The present study provided further evidence on the function and underlying mechanism of T lymphocyte subsets, which may be useful in the diagnosis and treatment of ankylosing spondylitis. D.A. Spandidos 2015-01 2014-11-04 /pmc/articles/PMC4247318/ /pubmed/25452811 http://dx.doi.org/10.3892/etm.2014.2046 Text en Copyright © 2015, Spandidos Publications http://creativecommons.org/licenses/by/3.0 This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited. |
spellingShingle | Articles WANG, CHENGGONG LIAO, QIANDE HU, YIHE ZHONG, DA T lymphocyte subset imbalances in patients contribute to ankylosing spondylitis |
title | T lymphocyte subset imbalances in patients contribute to ankylosing spondylitis |
title_full | T lymphocyte subset imbalances in patients contribute to ankylosing spondylitis |
title_fullStr | T lymphocyte subset imbalances in patients contribute to ankylosing spondylitis |
title_full_unstemmed | T lymphocyte subset imbalances in patients contribute to ankylosing spondylitis |
title_short | T lymphocyte subset imbalances in patients contribute to ankylosing spondylitis |
title_sort | t lymphocyte subset imbalances in patients contribute to ankylosing spondylitis |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4247318/ https://www.ncbi.nlm.nih.gov/pubmed/25452811 http://dx.doi.org/10.3892/etm.2014.2046 |
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