Literature DB >> 27931292

Circulating follicular T-helper cell subset distribution in patients with asthma.

Fang Gong1, Chunyan Qian, HuaYan Zhu, Jie Zhu, Yuhong Pan, QiaoJing Dong, DongLin Jiang.   

Abstract

BACKGROUND: The pathogenesis of allergic asthma is primarily characterized by abnormality in the immunoglobulin E (IgE) pathway, suggesting a possible role for follicular T-helper cells (Tfh) in the genesis of excessive IgE accumulation. The blood chemokine (C-X-C motif) receptor 5 (CXCR5)+CD4+ T cells, known as circulating Tfh, share common functional characteristics with Tfh cells from germinal centers. There are three subsets of circulating Tfh cells: Tfh1 (CXCR3+CC chemokine receptor [CCR] 6), Tfh2 (CXCR3CCR6) and Tfh17 (CXCR3CCR6+). However, data on circulating Tfh cell subsets distribution in patients with asthma are not available.
OBJECTIVE: To investigate the circulating Tfh cell subsets distribution in patients with asthma and to assess the relationship between Tfh cell subsets distribution and the serum IgE level.
METHODS: Thirty patients with severe allergic asthma and 30 age- and sex-matched healthy controls were enrolled in this study. The percentages and phenotypic assays of circulating Tfh cell subsets were assessed by flow cytometry. The total IgE levels were also measured. The correlation between the percentage of circulating Tfh cell subsets and the levels of serum total IgE was analyzed.
RESULTS: Our results showed polarization of Tfh2 cells within circulating Tfh cell subsets in the patients with asthma. Phenotypic assays showed that activated Tfh2 subtypes displayed the features of Tfh cells, including invariably coexpressed programmed cell death 1 (PD-1), and inducible costimulator (ICOS). Furthermore, not only the frequency of Tfh2 cells but also the ratio (%Tfh2/%Tfh1) positively correlated with the total IgE level in the blood.
CONCLUSION: Results of our data described an altered circulating Tfh subset distribution, which implied that this cell subset might play an important role in the pathogenesis of asthma.

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Year:  2016        PMID: 27931292     DOI: 10.2500/aap.2016.37.3982

Source DB:  PubMed          Journal:  Allergy Asthma Proc        ISSN: 1088-5412            Impact factor:   2.587


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