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Toxoplasma gondii Genotype Determines Tim-3 Expression Levels in Splenic and Circulatory T Cells in Mice
Toxoplasma gondii is an obligatory intracellular parasite that causes a common infection in many warm-blooded animals. During infection, the host’s immune system plays an important role in confining the dissemination of the parasites in the hosts. T cell immunoglobulin- and mucin domain–containing m...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6288189/ https://www.ncbi.nlm.nih.gov/pubmed/30564216 http://dx.doi.org/10.3389/fmicb.2018.02967 |
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author | Zhang, Yiwei Jiang, Ning Zhang, Ting Wang, Dawei Feng, Ying Sang, Xiaoyu Yang, Na Chen, Qijun |
author_facet | Zhang, Yiwei Jiang, Ning Zhang, Ting Wang, Dawei Feng, Ying Sang, Xiaoyu Yang, Na Chen, Qijun |
author_sort | Zhang, Yiwei |
collection | PubMed |
description | Toxoplasma gondii is an obligatory intracellular parasite that causes a common infection in many warm-blooded animals. During infection, the host’s immune system plays an important role in confining the dissemination of the parasites in the hosts. T cell immunoglobulin- and mucin domain–containing molecule 3 (Tim-3) has been characterized as an important regulator in cell-mediated immune responses in various infections. Here, we compared Tim-3 expression on splenic and circulatory T, B cells and a few cytokines in the sera of mice infected with the more virulent type I (RH) vs. the low virulent type II (ME49) strain. Tim-3 expression on the splenic and circulatory T cells of mice infected with T. gondii (RH strain) was higher than that in mice infected with T. gondii (ME49 strain). T. gondii infection reduced the proportion of splenic helper T cells (Th) and cytotoxic T cells (Tc) and increased Tim-3 expression. Further, serum levels of interleukin (IL)-2, interferon γ, tumor necrosis factor (TNF)-α, IL-12p70, IL-22, IL-17A, and IL-5 increased significantly after infection. Mice infected with T. gondii (ME49 strain) showed higher levels of TNF-α, IL-17A, IL-12p70, and IL-22 than that infected by the RH strain. Our study revealed that T. gondii strains may have their inherent ability in triggering different host immune responses, which may explain the clinical variation in diseases severity after infection. |
format | Online Article Text |
id | pubmed-6288189 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-62881892018-12-18 Toxoplasma gondii Genotype Determines Tim-3 Expression Levels in Splenic and Circulatory T Cells in Mice Zhang, Yiwei Jiang, Ning Zhang, Ting Wang, Dawei Feng, Ying Sang, Xiaoyu Yang, Na Chen, Qijun Front Microbiol Microbiology Toxoplasma gondii is an obligatory intracellular parasite that causes a common infection in many warm-blooded animals. During infection, the host’s immune system plays an important role in confining the dissemination of the parasites in the hosts. T cell immunoglobulin- and mucin domain–containing molecule 3 (Tim-3) has been characterized as an important regulator in cell-mediated immune responses in various infections. Here, we compared Tim-3 expression on splenic and circulatory T, B cells and a few cytokines in the sera of mice infected with the more virulent type I (RH) vs. the low virulent type II (ME49) strain. Tim-3 expression on the splenic and circulatory T cells of mice infected with T. gondii (RH strain) was higher than that in mice infected with T. gondii (ME49 strain). T. gondii infection reduced the proportion of splenic helper T cells (Th) and cytotoxic T cells (Tc) and increased Tim-3 expression. Further, serum levels of interleukin (IL)-2, interferon γ, tumor necrosis factor (TNF)-α, IL-12p70, IL-22, IL-17A, and IL-5 increased significantly after infection. Mice infected with T. gondii (ME49 strain) showed higher levels of TNF-α, IL-17A, IL-12p70, and IL-22 than that infected by the RH strain. Our study revealed that T. gondii strains may have their inherent ability in triggering different host immune responses, which may explain the clinical variation in diseases severity after infection. Frontiers Media S.A. 2018-12-04 /pmc/articles/PMC6288189/ /pubmed/30564216 http://dx.doi.org/10.3389/fmicb.2018.02967 Text en Copyright © 2018 Zhang, Jiang, Zhang, Wang, Feng, Sang, Yang and Chen. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Microbiology Zhang, Yiwei Jiang, Ning Zhang, Ting Wang, Dawei Feng, Ying Sang, Xiaoyu Yang, Na Chen, Qijun Toxoplasma gondii Genotype Determines Tim-3 Expression Levels in Splenic and Circulatory T Cells in Mice |
title | Toxoplasma gondii Genotype Determines Tim-3 Expression Levels in Splenic and Circulatory T Cells in Mice |
title_full | Toxoplasma gondii Genotype Determines Tim-3 Expression Levels in Splenic and Circulatory T Cells in Mice |
title_fullStr | Toxoplasma gondii Genotype Determines Tim-3 Expression Levels in Splenic and Circulatory T Cells in Mice |
title_full_unstemmed | Toxoplasma gondii Genotype Determines Tim-3 Expression Levels in Splenic and Circulatory T Cells in Mice |
title_short | Toxoplasma gondii Genotype Determines Tim-3 Expression Levels in Splenic and Circulatory T Cells in Mice |
title_sort | toxoplasma gondii genotype determines tim-3 expression levels in splenic and circulatory t cells in mice |
topic | Microbiology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6288189/ https://www.ncbi.nlm.nih.gov/pubmed/30564216 http://dx.doi.org/10.3389/fmicb.2018.02967 |
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