Expansion of a CD26low Effector TH Subset and Reduction in Circulating Levels of sCD26 in Stable Allergic Asthma in Adults

Nieto‐Fontarigo, Juan José; González-Barcala, FJ; San-José, ME; Cruz, María-Jesús; Liñares, Tania; Soto-Mera, M. T.; Valdés-Cuadrado, Luís; García-González, MA; Andrade-Bulos, LJ; Arias, Pilar; Nogueira, Marco Aurélio; Salgado, FJ

doi:10.18176/jiaci.0224

Cited by 8 publications

(9 citation statements)

References 26 publications

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“…A soluble version of CD26 (sCD26) has been found in the bloodstream as a free or a vesicle-associated protein [http://www.exocarta.org] 21 . Our previous in vitro studies evidenced a positive correlation between soluble DPP4 activity (an indirect measurement of sCD26) and CD26 expression on CD4 + cells 20 . Immune cells also appear to be a source of sCD26 in vivo 15 .…”

Section: Introductionmentioning

confidence: 87%

“…co-stimulation) 13–15 . Furthermore, CD26 high TH lymphocytes are considered memory 16,17 or activated cells 18 , which explains the presence of CD26 high CD4 + T cells in AA 19,20 . A soluble version of CD26 (sCD26) has been found in the bloodstream as a free or a vesicle-associated protein [http://www.exocarta.org] 21 .…”

Section: Introductionmentioning

confidence: 99%

“…However, contrary to our expectations, allergic asthmatics displayed higher membrane expression of CD26 on CD4 + T cells, but decreased levels of sCD26. This finding can be explained through the expansion of a “triple low” (Tlow; CD25 − CD127 − CD26 −/low ) subpopulation of effector T cells (Teff) 20 .…”

Section: Introductionmentioning

confidence: 99%

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Expansion of different subpopulations of CD26−/low T cells in allergic and non-allergic asthmatics

Nieto‐Fontarigo

Salgado

San-José

et al. 2019

Sci Rep

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CD26 displays variable levels between effector (TH 17 ≫ TH 1 > TH 2 > Treg) and naïve/memory (memory > naïve) CD4 + T lymphocytes. Besides, IL-6/IL − 6R is associated with TH 17 -differentiation and asthma severity. Allergic/atopic asthma (AA) is dominated by TH 2 responses, while TH 17 immunity might either modulate the TH 2 -dependent inflammation in AA or be an important mechanism boosting non-allergic asthma (NAA). Therefore, in this work we have compared the expression of CD26 and CD126 (IL-6Rα) in lymphocytes from different groups of donors: allergic (AA) and non-allergic (NAA) asthma, rhinitis, and healthy subjects. For this purpose, flow cytometry, haematological/biochemical, and in vitro proliferation assays were performed. Our results show a strong CD26-CD126 correlation and an over-representation of CD26 − subsets with a highly-differentiated effector phenotype in AA (CD4 + CD26 −/low T cells) and NAA (CD4 − CD26 − γδ-T cells). In addition, we found that circulating levels of CD26 (sCD26) were reduced in both AA and NAA, while loss of CD126 expression on different leukocytes correlated with higher disease severity. Finally, selective inhibition of CD26-mRNA translation led to enhanced T cell proliferation in vitro . These findings support that CD26 down-modulation could play a role in facilitating the expansion of highly-differentiated effector T cell subsets in asthma.

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Section: Introductionmentioning

confidence: 87%

Section: Introductionmentioning

confidence: 99%

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Expansion of different subpopulations of CD26−/low T cells in allergic and non-allergic asthmatics

Nieto‐Fontarigo

Salgado

San-José

et al. 2019

Sci Rep

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“…Studies have mentioned the relationship between DPP-4 inhibitors and infection [7,24], asthma [25], and lung injury [26]. Cluster of differentiation (CD) 26 might play a crucial role between DPP-4 inhibitors and immune regulation [27,28]. Higher levels of CD26 were equal to strongly activated T-cells and might cause potential immune-modulating effects in patients with DM [8].…”

Section: Discussionmentioning

confidence: 99%

Association between Dipeptidyl Peptidase-4 Inhibitors and Allergic Rhinitis in Asian Patients with Diabetes

Chen

et al. 2019

IJERPH

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In this retrospective study, we attempted to evaluate the association between dipeptidyl peptidase-4 (DPP-4) inhibitors and allergic rhinitis in patients with diabetes. We analyzed the Longitudinal Health Insurance Database 2000 subdatabase. Our study population included patients with type 2 diabetes (ICD-9-CM 250) between 2009 and 2012, and the study groups were DPP-4 inhibitor users and nonusers. Propensity scores were estimated in a multivariable logistic regression model for the analysis of allergic rhinitis (ICD-9-CM 477.9). Each group consisted of 6204 patients. DPP-4 inhibitor users had a reduced risk of allergic rhinitis (aHR = 0.74, 95% confidence interval (CI) = 0.61–0.90) in all stratifications. Among women, DPP-4 inhibitor users had a lower risk of allergic rhinitis (aHR = 0.67, 95% CI = 0.50–0.90). Among patients aged older than 40 years, DPP-4 inhibitor users had a decreased risk of allergic rhinitis (those aged 40–59: aHR = 0.75, 95% CI = 0.56–0.99; those aged ≧60: aHR = 0.73, 95% CI = 0.54–0.97). Among patients with comorbidities, the risk of allergic rhinitis for DPP-4 inhibitor users was 0.73 (95% CI = 0.60–0.90). High-dose (cumulative defined daily dose ≧648mg) DPP-4 inhibitor users had a decreased risk of allergic rhinitis (aHR = 0.23, 95% CI = 0.15–0.35). Our study revealed that Asian patients with diabetes who used DPP-4 inhibitors had decreased risk of allergic rhinitis, especially for DPP-4 inhibitor treatment in patients who were women, were older than 40 years, had higher diabetes severity scores, were taking higher doses of DPP-4 inhibitors, and had diabetes with comorbidities.

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“…Among them are B-type natriuretic peptide (BNP), playing a role in vasodilation [ 90 ]; substance P, a neurotransmitter [ 91 ]; peptide YY, which is involved in electrolyte absorption in the colon [ 92 ]; and neuropeptide Y (NPY), which is linked to learning and memory [ 93 ]. Moreover, DPP4 cleaves a variety of chemokines, which are all involved in chemotaxis and leukocyte recruitment, including interferon-inducible T cell α chemoattractant (ITAC) [ 94 ], interferon-γ-induced protein-10 (IP-10) [ 94 ], Eotaxin [ 95 ], monokine induced by interferon γ (MIG) [ 96 ], macrophage derived chemokine (MDC) [ 97 ], regulated on activation normal T cell expressed and presumably secreted (RANTES) [ 98 ], granulocyte colony stimulating factor (G-CSF) [ 99 ], granulocyte monocyte colony stimulating factor (GM-CSF) [ 99 ], and stromal-cell-derived factor-1 (SDF-1) [ 94 ]. For an overview of the DPP4 mediated effects see Table 1 .…”

Section: Molecular Functions Of Dipeptidyl-peptidase-4 (Dpp4)mentioning

confidence: 99%

Is there a Chance to Promote Arteriogenesis by DPP4 Inhibitors Even in Type 2 Diabetes? A Critical Review

Vedantham

Kluever²,

Deindl³

2018

Cells

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Cardiovascular diseases (CVD) are still the prevailing cause of death not only in industrialized countries, but even worldwide. Type 2 diabetes mellitus (type 2 DM) and hyperlipidemia, a metabolic disorder that is often associated with diabetes, are major risk factors for developing CVD. Recently, clinical trials proved the safety of gliptins in treating patients with type 2 DM. Gliptins are dipeptidyl-peptidase 4 (DPP4/CD26) inhibitors, which stabilize glucagon-like peptide-1 (GLP-1), thereby increasing the bioavailability of insulin. Moreover, blocking DPP4 results in increased levels of stromal cell derived factor 1 (SDF-1). SDF-1 has been shown in pre-clinical animal studies to improve heart function and survival after myocardial infarction, and to promote arteriogenesis, the growth of natural bypasses, compensating for the function of an occluded artery. Clinical trials, however, failed to demonstrate a superiority of gliptins compared to placebo treated type 2 DM patients in terms of cardiovascular (CV) outcomes. This review highlights the function of DPP4 inhibitors in type 2 DM, and in treating cardiovascular diseases, with special emphasis on arteriogenesis. It critically addresses the potency of currently available gliptins and gives rise to hope by pointing out the most relevant questions that need to be resolved.

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Expansion of a CD26low Effector TH Subset and Reduction in Circulating Levels of sCD26 in Stable Allergic Asthma in Adults

Cited by 8 publications

References 26 publications

Expansion of different subpopulations of CD26−/low T cells in allergic and non-allergic asthmatics

Expansion of different subpopulations of CD26−/low T cells in allergic and non-allergic asthmatics

Association between Dipeptidyl Peptidase-4 Inhibitors and Allergic Rhinitis in Asian Patients with Diabetes

Is there a Chance to Promote Arteriogenesis by DPP4 Inhibitors Even in Type 2 Diabetes? A Critical Review

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