CXCL10 antagonism and plasma sDPPIV correlate with increasing liver disease in chronic HCV genotype 4 infected patients

Ragab, Dina; Laird, Melissa E.; Duffy, Darragh; Casrouge, Armanda; Mamdouh, Rasha; Abass, Amal; Shenawy, Dina El.; Shebl, Abdelhadi M.; Elkashef, Wagdi; Zalata, Khaled; Kamal, Mostafa; Esmat, Gamal; Bonnard, Philippe; Fontanet, Arnaud; Rafik, Mona; Albert, Matthew L.

doi:10.1016/j.cyto.2013.04.016

Cited by 25 publications

(30 citation statements)

References 21 publications

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“…These data support the hypothesis that DPP4 serum enzymatic activity originates from the liver and is linked to insulin resistance [25, 28]. Previous studies reported that hepatitis C viral infections associated with higher DPP4a [29, 30]. In the current study, only one patient was concomitantly infected with hepatitis C virus (based on preoperative immunological results).…”

Section: Discussionsupporting

confidence: 89%

Prognostic value of plasma DPP4 activity in ST-elevation myocardial infarction

Chen²,

Chen³

et al. 2017

Cardiovasc Diabetol

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BackgroundDipeptidyl peptidase-4 (DPP4) regulates blood glucose levels and inflammation, and it is also implicated in the pathophysiological process of myocardial infarction (MI). Plasma DPP4 activity (DPP4a) may provide prognostic information regarding outcomes for ST-segment elevation MI (STEMI) patients.MethodsBlood samples were obtained from 625 consecutively admitted, percutaneous coronary intervention-treated STEMI patients with a mean age of 57 years old. DPP4a was quantified using enzymatic assays.ResultsThe median follow-up period was 30 months. Multivariate Cox-regression analyses (adjusted for confounding variables) showed that a 1 U/L increase of DPP4a did not associate with risks of major adverse cardiac or cerebrovascular events (MACCE), cardiovascular mortality, MI, heart failure readmission, stroke, non-cardiovascular mortality and repeated revascularization. However, in a subset of 149 diabetic STEMI patients, DPP4a associated with an increased risk of MACCE (HR 1.16; 95% CI 1.04–1.30; p = 0.01).ConclusionsDPP4a did not associate with cardiovascular events and non-cardiovascular mortality in non-diabetic STEMI patients. However, DPP4a may be associated with future MACCE in diabetic STEMI patients. Trial registration NCT03046576, registered on 5 February, 2017, retrospectively registeredElectronic supplementary materialThe online version of this article (doi:10.1186/s12933-017-0553-3) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 89%

Prognostic value of plasma DPP4 activity in ST-elevation myocardial infarction

Chen²,

Chen³

et al. 2017

Cardiovasc Diabetol

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“…IP‐10, a DPP IV/CD26 substrate inactivated by its proteolytic activity, is a chemotactic proinflammatory cytokine and chemoattractant for monocytes and T lymphocytes with the ability to inhibit the proliferation of endothelial cells . It has been shown that IP‐10 inhibits angiogenesis and delays reepithelialization of wounds .…”

Section: Discussionmentioning

confidence: 99%

Involvement of DPP IV/CD26 in cutaneous wound healing process in mice

Batičić

Pugel

Detel

et al. 2017

Wound Repair Regeneration

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Dipeptidyl peptidase IV (DPP IV/CD26) is a widely distributed multifunctional protein that plays a significant role in different physiological as well as pathological processes having a broad spectrum of bioactive substrates and immunomodulative properties. It has potential influence on different processes crucial for wound healing, including cell adhesion, migration, apoptosis, and extracellular matrix degradation. However, despite its known enzymatic and immunomodulative functions, limited data characterize the role of DPP IV/CD26 in cutaneous wound healing mechanisms. The aim of this study was to investigate the process of wound healing in conditions of CD26 deficiency in order to obtain better insights on the role of DPP IV/CD26 in cutaneous regeneration. Experimental wounds were made on the dorsal part of CD26 deficient (CD26 ) and wild-type mice (C57BL/6). The process of cutaneous wound healing was monitored on defined time schedule postwounding by macroscopic, microscopic, and biochemical analyses. Obtained results revealed a better rate of wound closure, revascularization and cell proliferation in CD26 mice, with enhanced local expression of hypoxia-inducible factor 1α and vascular endothelial growth factor. CD26 deficiency induced prompt macrophage recruitment at the site of skin damage but did not influence mobilization of T-cells in comparison with wild-type mice. CD26 mice have significantly higher values of IP-10 in serum and control skins compared with wild-type mice but values in wounds did not differ significantly on days 2, 4, and 7 of wound healing. DPP IV/CD26 activity was found to be decreased 4 days postwounding in serum and 2, 4, and 7 days postwounding in wounds of wild-type animals compared with control skins. These findings contribute to better understanding of wound healing mechanisms and could give a support in finding new therapeutic approaches for wound healing and tissue regeneration.

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“…Chronic HCV infection is strongly associated with an N-terminally truncated form of CXCL10, which inhibits Teff cell and NK cell chemotaxis to virally infected cells and tumors by antagonizing CXCR3-mediated signaling by biologically active CXCL10 (Casrouge et al, 2011;Riva et al, 2014). Antagonistic CXCL10 is generated through dipeptidylpeptidase 4 (DPP4)-mediated truncation of CXCL10, and both DPP4 and N-terminally truncated CXCL10 correlate with increasing liver disease and treatment failure in HCV patients (Casrouge et al, 2011;Ragab et al, 2013;Riva et al, 2014). It has been recently shown that in vivo post-translational processing of chemokines by DPP4 inhibits T cell migration to tumors and that DPP4 inhibition improves adjuvant-based immunotherapy, adoptive T cell transfer, and checkpoint blockade with anti-CTLA-4 and anti-PD-1 mAbs (Barreira da Silva et al, 2015).…”

Section: Background Chronic Infectionsmentioning

confidence: 97%

Resistance Mechanisms to Immune-Checkpoint Blockade in Cancer: Tumor-Intrinsic and -Extrinsic Factors

Pitt¹,

Vétizou²,

Daillère³

et al. 2016

Immunity

867

649

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Inhibition of immune regulatory checkpoints, such as CTLA-4 and the PD-1-PD-L1 axis, is at the forefront of immunotherapy for cancers of various histological types. However, such immunotherapies fail to control neoplasia in a significant proportion of patients. Here, we review how a range of cancer-cell-autonomous cues, tumor-microenvironmental factors, and host-related influences might account for the heterogeneous responses and failures often encountered during therapies using immune-checkpoint blockade. Furthermore, we describe the emerging evidence of how the strong interrelationship between the immune system and the host microbiota can determine responses to cancer therapies, and we introduce a concept by which prior or concomitant modulation of the gut microbiome could optimize therapeutic outcomes upon immune-checkpoint blockade.

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CXCL10 antagonism and plasma sDPPIV correlate with increasing liver disease in chronic HCV genotype 4 infected patients

Cited by 25 publications

References 21 publications

Prognostic value of plasma DPP4 activity in ST-elevation myocardial infarction

Prognostic value of plasma DPP4 activity in ST-elevation myocardial infarction

Involvement of DPP IV/CD26 in cutaneous wound healing process in mice

Resistance Mechanisms to Immune-Checkpoint Blockade in Cancer: Tumor-Intrinsic and -Extrinsic Factors

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