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      Association between cytokine profile and transcription factors produced by T‐cell subsets in early‐ and late‐onset pre‐eclampsia

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          Summary

          Pre‐eclampsia ( PE) is an obstetric pathology characterized by abnormal activation of the innate and adaptive immune systems dependent on the imbalance of T helper subsets. The present study aimed to evaluate the gene and protein expression of T helper type 1 (Th1)/Th2/Th17/regulatory T (Treg) cell transcription factors in peripheral blood lymphocytes from pregnant women with PE employing quantitative RTPCR and flow cytometry techniques, as well as the cytokine profile produced by these CD4 + T‐cell subsets in the plasma of pregnant women with PE, classified as early‐onset PE ( n = 20), late‐onset PE ( n = 20) and normotensive pregnant women ( n = 20). Results showed a higher percentage of CD4 + T cells expressing the RORc transcription factor (Th17) and a lower percentage of cells expressing FoxP3 (Treg) in women with early‐onset PE compared with late‐onset PE and normotensive groups. A lower gene expression of GATA‐3 transcription factor was detected in cells of women with early‐onset PE compared with the late‐onset PE group. Endogenous plasma levels of interleukin‐6 ( IL‐6), IL‐17 and tumour necrosis factor‐ α were significantly higher in the early‐onset PE group than in the late‐onset PE and normotensive groups, whereas IL‐4 (Th2 profile) and IL‐22 (Th17 profile), were not significantly different between the studied groups. The endogenous levels of transforming growth factor‐ β and IL‐10 were significantly lower in the pre‐eclamptic than in the normotensive groups of the same gestational age, with a significant difference between early‐ and late‐onset PE. The results show that in women with PE there is an imbalance between inflammatory and anti‐inflammatory profiles in CD4 + T‐cell subsets, with polarization to Th17 profiles in the early‐onset PE, considered as the severe form of PE.

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          Author and article information

          Contributors
          peracoli@ibb.unesp.br
          Journal
          Immunology
          Immunology
          10.1111/(ISSN)1365-2567
          IMM
          Immunology
          John Wiley and Sons Inc. (Hoboken )
          0019-2805
          1365-2567
          19 June 2017
          September 2017
          : 152
          : 1 ( doiID: 10.1111/imm.2017.152.issue-1 )
          : 163-173
          Affiliations
          [ 1 ] Department of Gynaecology and Obstetrics Medical School Botucatu Sao Paulo State University (UNESP) Botucatu Sao Paulo Brazil
          [ 2 ] Department of Microbiology and Immunology Institute of Biosciences Botucatu Sao Paulo State University (UNESP) Botucatu Sao Paulo Brazil
          Author notes
          [*] [* ] Correspondence: Maria Terezinha Serrao Peracoli, Department of Microbiology and Immunology, Institute of Biosciences, Rubiao Junior s/n, UNESP, Botucatu, Sao Paulo, CEP 18618‐691 Brazil. Email: peracoli@ 123456ibb.unesp.br

          Senior author: Maria Terezinha Serrao Peracoli

          Author information
          http://orcid.org/0000-0002-8990-0237
          http://orcid.org/0000-0002-0936-9512
          Article
          PMC5543493 PMC5543493 5543493 IMM12757
          10.1111/imm.12757
          5543493
          28502089
          700b0c21-cd0d-4b01-a191-42a4033f00f9
          © 2017 John Wiley & Sons Ltd
          History
          : 18 January 2017
          : 18 April 2017
          : 06 May 2017
          Page count
          Figures: 5, Tables: 2, Pages: 11, Words: 7920
          Funding
          Funded by: Fundação do Amparo à Pesquisa do Estado de São Paulo, Brazil, FAPESP
          Award ID: 2012/24697‐8
          Award ID: 2014/25124‐7
          Categories
          Original Article
          Original Articles
          Custom metadata
          2.0
          imm12757
          September 2017
          Converter:WILEY_ML3GV2_TO_NLMPMC version:5.1.6 mode:remove_FC converted:04.08.2017

          transcription factors,cytokines,regulatory T cells,reproductive immunology,T cells

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