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See detailAsthma-related inflammation promotes lung metastasis of breast cancer cells through CCL11–CCR3 pathway
BEKAERT, Sandrine ULiege; Rocks, Natacha ULiege; Vanwinge, Céline ULiege et al

in Respiratory Research (2021), 22(1), 61

Background: Mechanisms that preclude lung metastasis are still barely understood. The possible consequences of allergic airways inflammation on cancer dissemination were studied in a mouse model of breast ... [more ▼]

Background: Mechanisms that preclude lung metastasis are still barely understood. The possible consequences of allergic airways inflammation on cancer dissemination were studied in a mouse model of breast cancer. Methods: Balb/c mice were immunized and daily exposed to ovalbumin (OVA) from day 21. They were subcutane- ously injected with 4T1 mammary tumor cells on day 45 and sacrificed on day 67. Lung metastases were measured by biophotonic imaging (IVIS 200 Imaging System) and histological measurement of tumor area (Cytomine software). Effects of CCL11 were assessed in vivo by intratracheal instillations of recCCL11 and in vitro using Boyden chambers. CCR3 expression on cell surface was assessed by flow cytometry. Results: The extent of tumor metastases was significantly higher in lungs of OVA-exposed mice and increased levels of CCL11 expression were measured after OVA exposure. Migration of 4T1 cells and neutrophils was stimulated in vitro and in vivo by recCCL11. 4T1 cells and neutrophils express CCR3 as shown by flow cytometry and a selective CCR3 antagonist (SB-297006) inhibited the induction of 4T1 cells migration and proliferation in response to recCCL11. Conclusions: Allergic inflammation generated by exposure to allergens triggers the implantation of metastatic cells from primary breast tumor into lung tissues plausibly in a CCL11–CCR3-dependent manner. This indicates that asthma related inflammation in lungs might be a risk factor for lung metastasis in breast cancer patients. [less ▲]

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See detailSevere asthma: oral corticosteroid alternatives and the need for optimal referral pathways
CATALDO, Didier ULiege; LOUIS, Renaud ULiege; MICHILS, Alain et al

in Journal of Asthma (2021)

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See detailExpert Consensus on the Tapering of Oral Corticosteroids for the Treatment of Asthma. A Delphi Study.
Suehs, Carey M.; Menzies-Gow, Andrew; Price, David et al

in American journal of respiratory and critical care medicine (2021), 203(7), 871-881

Rationale: There is a need to minimize oral corticosteroid (OCS) use in patients with asthma to prevent their costly and burdensome adverse effects. Current guidelines do not provide recommendations for ... [more ▼]

Rationale: There is a need to minimize oral corticosteroid (OCS) use in patients with asthma to prevent their costly and burdensome adverse effects. Current guidelines do not provide recommendations for OCS tapering in patients with asthma.Objectives: To develop expert consensus on OCS tapering among international experts.Methods: A modified Delphi method was used to develop expert consensus statements relating to OCS use, tapering, adverse effects, adrenal insufficiency, and patient-physician shared decision-making. Initial statements proposed by experts were categorized, filtered for repetition, and presented back to experts over three ranking rounds to obtain consensus (≥70% agreement).Measurements and Main Results: One hundred thirty-one international experts participated in the study, and 296 statements were ranked. Numerous recommendations and guidance regarding appropriate OCS use were established. Experts agreed that OCS tapering should be attempted in all patients with asthma receiving maintenance OCS therapy, with personalization of tapering rhythm and speed. The importance of recognizing individual adverse effects was also established; however, a unified approach to the assessment of adrenal insufficiency was not reached. Shared decision-making was considered an important goal during the tapering process.Conclusions: In this Delphi study, expert consensus statements were generated on OCS use, tapering, adverse-effect screening, and shared decision-making, which may be used to inform clinical practice. Areas of nonconsensus were identified, highlighting uncertainty among the experts around some aspects of OCS use in asthma, such as adrenal insufficiency, which underscores the need for further research in these domains. [less ▲]

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See detailNeutrophil extracellular traps infiltrate the lung airway, interstitial, and vascular compartments in severe COVID-19
Radermecker, Coraline ULiege; Detrembleur, Nancy ULiege; Guiot, Julien ULiege et al

in Journal of Experimental Medicine (2020), 217(12),

Infection with SARS-CoV-2 is causing a deadly and pandemic disease called coronavirus disease-19 (COVID-19). While SARS-CoV-2-triggered hyperinflammatory tissue-damaging and immunothrombotic responses are ... [more ▼]

Infection with SARS-CoV-2 is causing a deadly and pandemic disease called coronavirus disease-19 (COVID-19). While SARS-CoV-2-triggered hyperinflammatory tissue-damaging and immunothrombotic responses are thought to be major causes of respiratory failure and death, how they relate to lung immunopathological changes remains unclear. Neutrophil extracellular traps (NETs) can contribute to inflammation-associated lung damage, thrombosis, and fibrosis. However, whether NETs infiltrate particular compartments in severe COVID-19 lungs remains to be clarified. Here we analyzed postmortem lung specimens from four patients who succumbed to COVID-19 and four patients who died from a COVID-19-unrelated cause. We report the presence of NETs in the lungs of each COVID-19 patient. NETs were found in the airway compartment and neutrophil-rich inflammatory areas of the interstitium, while NET-prone primed neutrophils were present in arteriolar microthrombi. Our results support the hypothesis that NETs may represent drivers of severe pulmonary complications of COVID-19 and suggest that NET-targeting approaches could be considered for the treatment of uncontrolled tissue-damaging and thrombotic responses in COVID-19. © 2020 Radermecker et al. This article is distributed under the terms of an Attribution-Noncommercial-Share Alike-No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution-Noncommercial-Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/). [less ▲]

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See detailADAM28: Another ambivalent protease in cancer
Hubeau, Céline ULiege; Rocks, Natacha ULiege; Cataldo, Didier ULiege

in Cancer Letters (2020), 494

Emergence of novel therapeutic options in a perspective of personalized therapy of cancer relies on the discovery of precise molecular mechanisms involved in the switch from a localized tumor to invasive ... [more ▼]

Emergence of novel therapeutic options in a perspective of personalized therapy of cancer relies on the discovery of precise molecular mechanisms involved in the switch from a localized tumor to invasive metastasis spread. Pro-tumor functions have been mostly ascribed to proteolytic enzymes from the metalloproteinase family including A Disintegrin And Metalloproteinases (ADAMs). Particularly, when expressed by cancer cells, ADAM28 protease supports cancer cell proliferation, survival and migration as well as metastatic progression. In sharp contrast, ADAM28 derived from the tumor microenvironment has shown to exert strong protective effects against deleterious metastasis dissemination. Indeed, depletion of host-derived ADAM28 (ADAM28 KO mice) accelerates colonization lung tissues, increases tumor foci implantation, and impairs T cell immune response. In this review, we outline specific ADAM28 functions when specifically expressed by carcinoma cells or by tumor microenvironment. Finally, we discuss about future research strategies that could be pursued to highlight new functions of this protease in cancer. © 2020 Elsevier B.V. [less ▲]

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See detailMaternal asthma is associated with persistent changes in allergic offspring antibody glycosylation
Sodemann, Elisa B.; Dähling, Sabrina; Klopfleisch, Robert et al

in Clinical & Experimental Allergy (2020), 50

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See detailMicroenvironment-derived ADAM28 impacts the onset of lung cancer
Hubeau, Céline ULiege; Gérard, Catherine ULiege; Carnet, Oriane ULiege et al

Poster (2019, September)

Background ADAM28 expression is upregulated in non-small cell lung carcinoma and correlated with cell proliferation and metastatic dissemination. Moreover, in vivo studies have shown that knockdown of ... [more ▼]

Background ADAM28 expression is upregulated in non-small cell lung carcinoma and correlated with cell proliferation and metastatic dissemination. Moreover, in vivo studies have shown that knockdown of ADAM28 in tumor cells decreased the primary tumor growth and formation of lung metastasis. Besides, ADAM28 is thought to be an important regulator of inflammatory signaling pathways as it sheds the pro-inflammatory cytokine, pro-TNF-alpha. ADAM28 protease also interacts with integrins and the P-selectin glycoprotein ligand-1 leading to inflammatory cell migration. Altogether, these findings suggest that ADAM28 contributes to cellular mechanisms leading to cancer development and progression. Methods This study aims to characterize the effects of microenvironment-derived ADAM28 on lung metastasis formation. To achieve this purpose, we generated ADAM28-/- mice into two different mouse strains (C57BL/6 and BALB/c). Lung metastatic dissemination was assessed in both ADAM28-/- and wild-type (WT) mice after intravenous injection of Lewis Lung Carcinoma cells, B16K1 melanoma cells or 4T1 breast carcinoma cells. As ADAM28 promotes leukocyte transendothelial migration, lymphocyte subtypes implicated in tumor cytotoxicity or in regulation of immune response were studied by flow cytometry. Results An unexpected increased tumor burden was found in lungs of ADAM28-/- mice as compared to WT mice. Flow cytometry analysis revealed that less CD8+ T were infiltrated within lungs of ADAM28-/- tumor-bearing mice. Moreover, a reduced CD8+ T cell population was observed in the spleen of naïve ADAM28-/- mice that is not caused by an impaired T cell maturation in the thymus. Ex vivo assays demonstrated that intrinsic properties of CD8+ T cells from ADAM28-/- mice were not affected by ADAM28 deficiency as their proliferation, migration and activation was similar. Besides, we found no expression of ADAM28 in isolated CD8+ T cells from the spleen of ADAM28-/- and WT mice. Therefore, we hypothesized that ADAM28 indirectly modulates the anti-tumor cytotoxic immune response. We also found that ADAM28 depletion is associated with a reduced infiltration of NK cell within lungs of ADAM28-/- tumor-bearing mice. Conclusion Our results demonstrate a protective effect of microenvironment-derived ADAM28 by regulating the tumor-associated immune response. [less ▲]

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See detailStromal integrin alpha11 regulates PDGFR-beta signaling and promotes breast cancer progression.
Primac, Irina ULiege; Maquoi, Erik ULiege; Blacher, Silvia ULiege et al

in Journal of Clinical Investigation (2019), 130

Cancer-associated fibroblasts (CAFs) are key actors in modulating the progression of many solid tumors such as breast cancer (BC). Herein, we identify an integrin alpha11/PDGFRbeta+ CAF subset displaying ... [more ▼]

Cancer-associated fibroblasts (CAFs) are key actors in modulating the progression of many solid tumors such as breast cancer (BC). Herein, we identify an integrin alpha11/PDGFRbeta+ CAF subset displaying tumor-promoting features in BC. In the preclinical MMTV-PyMT mouse model, integrin alpha11-deficiency led to a drastic reduction of tumor progression and metastasis. A clear association between integrin alpha11 and PDGFRbeta was found at both transcriptional and histological levels in BC specimens. High stromal integrin alpha11/PDGFRbeta expression was associated with high grades and poorer clinical outcome in human BC patients. Functional assays using five CAF subpopulations (one murine, four human) revealed that integrin alpha11 promotes CAF invasion and CAF-induced tumor cell invasion upon PDGF-BB stimulation. Mechanistically, integrin alpha11 pro-invasive activity relies on its ability to interact with PDGFRbeta in a ligand-dependent manner and to promote its downstream JNK activation, leading to the production of tenascin C, a pro-invasive matricellular protein. Pharmacological inhibition of PDGFRbeta and JNK impaired tumor cell invasion induced by integrin alpha11-positive CAFs. Collectively, our study uncovers an integrin alpha11-positive subset of pro-tumoral CAFs that exploits PDGFRbeta/JNK signalling axis to promote tumor invasiveness in BC. [less ▲]

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See detailMethod for increasing the bioavailability of inhaled compounds
Vanbever, Rita; Koussoroplis, Salome; Cataldo, Didier ULiege et al

Patent (2019)

The present invention relates to a compound comprising one or more PEG moieties , wherein said compound is a therapeutic agent active for treating a respiratory disease . The present invention also ... [more ▼]

The present invention relates to a compound comprising one or more PEG moieties , wherein said compound is a therapeutic agent active for treating a respiratory disease . The present invention also relates to a method for preventing and / or treating a respiratory disease in a subject in need thereof comprising the administration of a PEGylated therapeutic agent. Another object of the invention is a method for enhancing the bioavailability of a therapeutic agent , for enhancing the pulmonary residency of a therapeutic agent and / or for reducing the pulmonary clearance of a therapeutic agent , wherein said methods comprise the PEGylation of the therapeutic agent . [less ▲]

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See detailOzone-primed neutrophils promote early steps of tumor cell metastasis to lungs by enhancing their NET production
Rocks, Natacha ULiege; Vanwinge, Céline ULiege; Radermecker, Coraline ULiege et al

in Thorax (2019), 0

Air pollution, including particulates and gazes such as ozone (O3), is detrimental for patient’s health and has repeatedly been correlated to increased morbidity and mortality in industrialized countries ... [more ▼]

Air pollution, including particulates and gazes such as ozone (O3), is detrimental for patient’s health and has repeatedly been correlated to increased morbidity and mortality in industrialized countries. Although studies have described a link between ambient particulate matter and increased lung cancer morbidity, no direct relation has yet been established between O3 exposure and metastatic dissemination to lungs. [less ▲]

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See detailADAM10 mediates malignant pleural mesothelioma invasiveness
Sepult, Christelle ULiege; Bellefroid, Marine ULiege; Rocks, Natacha ULiege et al

in Oncogene (2019)

Malignant pleural mesothelioma (MPM) is an aggressive cancer with limited therapeutic options and treatment efficiency. Even if the latency period between asbestos exposure, the main risk factor, and ... [more ▼]

Malignant pleural mesothelioma (MPM) is an aggressive cancer with limited therapeutic options and treatment efficiency. Even if the latency period between asbestos exposure, the main risk factor, and mesothelioma development is very long, the local invasion of mesothelioma is very rapid leading to a mean survival of one year after diagnosis. ADAM10 (A Disintegrin And Metalloprotease) sheddase targets membrane-bound substrates and its overexpression is associated with progression in several cancers. However, nothing is known about ADAM10 implication in MPM. In this study, we demonstrated higher ADAM10 expression levels in human MPM as compared to control pleural samples and in human MPM cell line. This ADAM10 overexpression was also observed in murine MPM samples. Two mouse mesothelioma cell lines were used in this study including one primary cell line obtained by repeated asbestos fibre injections. We show, in vitro, that ADAM10 targeting through shRNA and pharmacological (GI254023X) approaches reduced drastically mesothelioma cell migration and invasion, as well as for human mesothelioma cells treated with siRNA targeting ADAM10. Moreover, ADAM10 downregulation in murine mesothelioma cells significantly impairs MPM progression in vivo after intrapleural cell injection. We also demonstrate that ADAM10 sheddase downregulation decreases the production of a soluble N-cadherin fragment through membrane N-cadherin, which stimulated mesothelioma cell migration. Taken together, we demonstrate that ADAM10 is overexpressed in MPM and takes part to MPM progression through the generation of N-cadherin fragment that stimulates mesothelioma cell migration. ADAM10 inhibition is worth considering as a therapeutic perspective in mesothelioma context. [less ▲]

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See detailLocally instructed CXCR4(hi) neutrophils trigger environment-driven allergic asthma through the release of neutrophil extracellular traps.
Radermecker, Coraline ULiege; Sabatel, Catherine ULiege; Vanwinge, Céline ULiege et al

in Nature Immunology (2019)

Low exposure to microbial products, respiratory viral infections and air pollution are major risk factors for allergic asthma, yet the mechanistic links between such conditions and host susceptibility to ... [more ▼]

Low exposure to microbial products, respiratory viral infections and air pollution are major risk factors for allergic asthma, yet the mechanistic links between such conditions and host susceptibility to type 2 allergic disorders remain unclear. Through the use of single-cell RNA sequencing, we characterized lung neutrophils in mice exposed to a pro-allergic low dose of lipopolysaccharide (LPS) or a protective high dose of LPS before exposure to house dust mites. Unlike exposure to a high dose of LPS, exposure to a low dose of LPS instructed recruited neutrophils to upregulate their expression of the chemokine receptor CXCR4 and to release neutrophil extracellular traps. Low-dose LPS-induced neutrophils and neutrophil extracellular traps potentiated the uptake of house dust mites by CD11b(+)Ly-6C(+) dendritic cells and type 2 allergic airway inflammation in response to house dust mites. Neutrophil extracellular traps derived from CXCR4(hi) neutrophils were also needed to mediate allergic asthma triggered by infection with influenza virus or exposure to ozone. Our study indicates that apparently unrelated environmental risk factors can shape recruited lung neutrophils to promote the initiation of allergic asthma. [less ▲]

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See detailPreclinical evaluation of topically-administered PEGylated Fab’ lung toxicity
Freches, D.; Rocks, Natacha ULiege; Patil, H. P. et al

in International Journal of Pharmaceutics: X (2019), 1

PEGylation is a promising approach to increase the residence time of antibody fragments in the lungs and sustain their therapeutic effects. However, concerns arise as to the potential pulmonary toxicity ... [more ▼]

PEGylation is a promising approach to increase the residence time of antibody fragments in the lungs and sustain their therapeutic effects. However, concerns arise as to the potential pulmonary toxicity of antibody fragments conjugated to high molecular weight (HMW) polyethylene glycol (PEG), notably after repeated administrations, and the possibility of PEG accumulation in the lungs. The purpose of this proof-of-concept study is to give insights about the safety of lung administration of a Fab’ anti-IL17A antibody fragment conjugated to two-armed 40 kDa PEG (PEG40). The presence of the PEG40 moiety inside alveolar macrophages remained stable for at least 24 h after intratracheal administration of PEG40-Fab’ to mice. PEG40 was then progressively cleared from alveolar macrophages. Incubation of PEG40 alone with macrophages in vitro did not significantly harm macrophages and did not affect phagocytosis or the production of inflammatory markers. After acute or chronic administration of PEG40-Fab’ to mice, no signs of significant pulmonary toxicity or inflammatory cell accumulation were observed. A vacuolization of alveolar macrophages not associated with any inflammation was noticed when PEG40, PEG40-Fab’, or unPEGylated Fab’ were administered. To conclude this preliminary proof of concept study, acute or repeated pulmonary administrations of PEGylated Fab’ appear safe in rodents. © 2019 The Authors [less ▲]

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See detailLymph/angiogenesis contributes to sex differences in lung cancer through oestrogen receptor alpha signalling
Dubois, Charline; Rocks, Natacha ULiege; Blacher, Silvia ULiege et al

in Endocrine-Related Cancer (2019), 26(2), 201-216

Oestrogen signalling pathways are emerging targets for lung cancer therapy. Unravelling the contribution of oestrogens in lung cancer development is a pre-requisite to support the development of sex-based ... [more ▼]

Oestrogen signalling pathways are emerging targets for lung cancer therapy. Unravelling the contribution of oestrogens in lung cancer development is a pre-requisite to support the development of sex-based treatments and identify patients who could potentially benefit from anti-oestrogen treatments. In this study, we highlight the contribution of lymphatic and blood endothelia in the sex-dependent modulation of lung cancer. The orthotopic graft of syngeneic lung cancer cells into immunocompetent mice showed that lung tumours grow faster in female mice than in males. Moreover, oestradiol (E2) promoted tumour development, increased lymph/angiogenesis and VEGFA and bFGF levels in lung tumours of females through an oestrogen receptor (ER) alpha-dependent pathway. Furthermore, while treatment with ERb antagonist was inefficient, ERa antagonist (MPP) and tamoxifen decreased lung tumour volumes, altered blood and lymphatic vasculature and reduced VEGFA and bFGF levels in females, but not in males. Finally, the quantification of lymphatic and blood vasculature of lung adenocarcinoma biopsies from patients aged between 35 and 55 years revealed more extensive lymphangiogenesis and angiogenesis in tumour samples issued from women than from men. In conclusion, our findings highlight an E2/ERa-dependent modulation of lymphatic and blood vascular components of lung tumour microenvironment. Our study has potential clinical implication in a personalised medicine perspective by pointing to the importance of oestrogen status or supplementation on lung cancer development that should be considered to adapt therapeutic strategies. [less ▲]

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See detailRelationship between peak expiratory flow and incidence of frailty, deaths and falls among nursing home residents: Results of the SENIOR cohort
Charles, Alexia ULiege; Buckinx, Fanny ULiege; Cataldo, Didier ULiege et al

in Archives of Gerontology and Geriatrics (2019), 85

Objective: To correlate peak expiratory flow (PEF) with the incidence of frailty, deaths and falls among nursing home residents. Methods: This is a 1-year longitudinal analysis performed on the clinical ... [more ▼]

Objective: To correlate peak expiratory flow (PEF) with the incidence of frailty, deaths and falls among nursing home residents. Methods: This is a 1-year longitudinal analysis performed on the clinical data of the SENIOR cohort. PEF, measured by peak flow meter, was considered as “low” when the observed value was ≤80% of the theoretical value. Physical capacity was evaluated using Short Physical Performance Battery, balance and gait using Tinetti test and muscle strength using a dynamometer. The incidence of frailty was defined as the transition from a “robust” or “prefrail” status to a “frail” status following Fried's criteria. Deaths and falls were also collected. Results: Among 646 subjects included at baseline (83.2 ± 9 years and 72.1% women), 297 (45.7%) displayed a low PEF. In this subgroup, physical capacity (p-values from 0.01 to <0.001), muscle strength (p < 0.001), balance and gait score (p < 0.001) were significantly lower compared to subjects displaying normal PEF. Subjects who became frail after one year displayed a lower % of the theoretical PEF value compared to those that did not (88.52 ± 45.06 vs 102.78 ± 50.29, respectively, p = 0.03). After adjustment for potential confounding variables (calf circumference, Tinetti test, SPPB test and handgrip strength), PEF was no longer associated with the occurrence of frailty. There was no association between PEF and mortality and falls. Conclusion: In a nursing home setting, PEF is not an independent factor associated with the incidence of frailty, deaths and falls. © 2019 Elsevier B.V. [less ▲]

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See detailADAM28 deletion in mice impacts lung metastasis formation
Hubeau, Céline ULiege; Gerard, Catherine; Carnet, Oriane ULiege et al

Conference (2018, September 19)

ADAM28 expression is upregulated in non-small cell lung carcinoma and correlated with cell proliferation and metastatic dissemination. In addition, ADAM28 is thought to be an important regulator of ... [more ▼]

ADAM28 expression is upregulated in non-small cell lung carcinoma and correlated with cell proliferation and metastatic dissemination. In addition, ADAM28 is thought to be an important regulator of inflammatory signaling pathways as this protease shed the pro-inflammatory cytokine, pro-TNF-alpha. ADAM28 also interacts with integrins and a P-selectin ligand (PSGL-1) involved in inflammatory cell migration. All these findings suggest that ADAM28 contributes to cancer development and progression. This project aims to characterize the effects of host-derived ADAM28 on lung metastasis formation using an ADAM28-/- mouse model. Lewis Lung Carcinoma cells and B16K1 melanoma cells were intravenously injected in ADAM28-/- and wild-type (WT) mice. An unexpected increased tumor development was found in lungs of ADAM28-/- mice. As ADAM28 is associated with lymphocyte transendothelial migration, lymphocyte subtypes implicated in tumor cytotoxicity or in regulation of immune response were studied by flow cytometry. Results showed that less CD8+ T and NK cells were infiltrated within lungs of ADAM28-/- tumor-bearing mice as compared to WT mice. Moreover, less CD8+ T cells were counted within the spleen of naïve ADAM28-/- mice. These data were confirmed in a mouse model where 4T1 breast carcinoma cells were intravenously injected in ADAM28-/- BALB/c mice. Intrinsic properties of CD8+ T cells from ADAM28-/- mice were not affected by ADAM28 depletion as they were able to proliferate, to be activated and to migrate. Further investigations are required to explain the CD8+ T cell phenotype in ADAM28-deficient mice. Our results suggest a protective effect of ADAM28 derived from the host microenvironment by indirectly regulate the immune response. [less ▲]

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See detailNEUTROPHIL EXTRACELLULAR TRAPS AS MAJOR DETERMINANTS OF ASTHMA
Radermecker, Coraline ULiege; Sabatel, Catherine ULiege; Vanwinge, Céline ULiege et al

Conference (2018, September)

Detailed reference viewed: 36 (2 ULiège)
See detailAnti-metastatic effect of ADAM28 derived from the microenvironment
Gérard, Catherine ULiege; Rocks, Natacha ULiege; Carnet, Oriane ULiege et al

Poster (2018, July 01)

Detailed reference viewed: 33 (12 ULiège)