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Expansion of a CD26low effector TH subset and reduction of circulating levels of sCD26 in stable allergic asthma in adults

Nieto-Fontarigo JJ1, González-Barcala FJ2, San-José ME3, Cruz MJ4, Linares T5, Soto-Mera MT5, Valdés L6, García-González MA7, Andrade-Bulos LJ1, Arias P1, Nogueira M1, Salgado FJ1

1Department of Biochemistry and Molecular Biology, Faculty of Biology-Biological Research Centre (CIBUS), Universidad de Santiago de Compostela, Santiago de Compostela, Spain.
2Department of Medicine-University of Santiago de Compostela, Spanish Biomedical Research Networking Centre-CIBERES, Department of Respiratory Medicine-University Hospital of Santiago de Compostela, Health Research Institute of Santiago de Compostela (IDIS).
3Clinical Analysis Service, USC University Hospital Complex (CHUS), Santiago de Compostela, Spain.
4Department of Respiratory Medicine-Hospital Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. Spanish Biomedical Research Networking Centre-CIBERES.
5Allergy Department, University Hospital of Pontevedra (CHOP), Pontevedra, Spain.
6Department of Medicine-University of Santiago de Compostela, Department of Respiratory Medicine-University Hospital of Santiago de Compostela, Health Research Institute of Santiago de Compostela (IDIS).
7Laboratory of Nephrology, Sanitary Research Institute (IDIS), Santiago de Compostela, Spain.

J Investig Allergol Clin Immunol 2018; Vol. 28(2)
doi: 10.18176/jiaci.0224

Background: Asthma pathogenesis is dependent on the balance between regulatory and effector T cells, which display differential expression of CD25 and CD26. Therefore, alteration of circulating levels of sCD25 and sCD26 during allergic asthma could be conditioned by leukocyte phenotype changes.
Objectives: To analyse CD25 and CD26 expression on T lymphocytes and their soluble derivatives (sCD25, sCD26) during stable phases of moderate-severe allergic asthma.
Methods: Cross-sectional study with two adult cohorts of allergic asthmatics. Clinical, anthropometric, lung function, haematological and biochemical parameters were measured. Flow cytometry phenotyping was done in both circulating and cultured leukocytes. Dipeptidyl peptidase 4 (DPP4) activity was assayed in culture supernatants.
Results: In vitro studies showed an up-regulation of CD26 on human T lymphocytes upon activation, especially by TH17-favouring conditions, and a correlation with soluble DPP4 activity (rs=0.641; P < 0.001). CD26 expression on lymphocytes was higher in asthmatics, while serum sCD26 was lower in women and patients. The last finding could be related with an expanded CD25low/CD26low/CD127low subset of effector CD4+ T cells in allergic asthma, without changes in Treg percentages. However, women showed an increased Teff/Treg ratio, which could explain their higher susceptibility to asthma.
Conclusions: Allergic asthma causes an increment in CD25lowCD26low TH cells detected in stable stages. These changes are mirrored in serum and should be considered in the light of the down-modulating role of CD26 on important chemokines related to asthma pathogenesis such as CCL11 (eotaxin), CCL5 (RANTES) or CXCL12a (SDF-1α).

Key words: Asthma biomarkers, CD25, CD26, DPP4, Lymphocytes, T helper cells

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