References of "Marichal, Thomas"
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See detailCharacterization and regulation of the intestinal epithelial cell response to colitogenic triggers
El Abbas, Sophie ULiege; Beguin, C; Schyns, Joey ULiege et al

in Proceedings of Annual meeting of the French Society for Immunology (SFI) (2017, November 07)

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See detailRab guanine nucleotide exchange factor 1 (Rabgef1) restricts intestinal inflammation by limiting pro-inflammatory signals in Intestinal Epithelial Cells (IECs)
El Abbas, Sophie ULiege; Beguin, Charline ULiege; Schyns, Joey ULiege et al

in Proceedings: 4th FARAH-DAY (2017, October 13)

Rab guanine nucleotide exchange factor (GEF-)1 (Rabgef1), a multifunctional protein whose in vivo functions remained unknown until recently, is highly expressed in mouse and human epithelial cells. The ... [more ▼]

Rab guanine nucleotide exchange factor (GEF-)1 (Rabgef1), a multifunctional protein whose in vivo functions remained unknown until recently, is highly expressed in mouse and human epithelial cells. The aim of this study is to investigate the role of Rabgef1 in intestinal epithelial cells (IECs) and intestinal homeostasis in mice. We performed conditional deletion of Rabgef1 gene using the cre-lox system to obtain mice lacking Rabgef1 specifically in IECs (Rabgef1IEC-KO), under the wild-type (WT) or the colitis-prone Interleukin-10 (Il-10)-deficient background. In addition, we used the CRISPR-Cas9 technology to obtain a murine IEC line deficient in Rabgef1. Rabgef1IEC-KO mice under the WT background did not develop spontaneous intestinal abnormalities but exhibited an altered intestinal microbial composition associated with minor changes in IEC pro-inflammatory gene expression profile. Moreover, Rabgef1IEC-KO mice exhibited an increased susceptibility to inflammation in a dextran sodium sulfate (DSS)-induced model of colitis under the WT background, as well as in a constitutive model of colitis under the Il-10-¬deficient background. In vitro, we showed that mouse IECs lacking Rabgef1 significantly overexpressed several pro-inflammatory cytokines and chemokines as compared to control cells. Taken together, these results support that Rabgef1 acts as a regulator of intestinal homeostasis and inflammation, and that dysregulated Rabgef1 expression could contribute to intestinal barrier dysfunction in inflammatory conditions of the gut. [less ▲]

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See detailRelease of Neutrophils Extracellular Traps as a main trigger for asthma onset
Radermecker, Coraline ULiege; Sabatel, Catherine ULiege; Toussaint, Marie et al

Poster (2017, June 20)

Allergic asthma is an important Th2 associated immunopathology. Even if the pathology of the disease is well described, its etiology is still largely unknown. Nevertheless, some environmental factors like ... [more ▼]

Allergic asthma is an important Th2 associated immunopathology. Even if the pathology of the disease is well described, its etiology is still largely unknown. Nevertheless, some environmental factors like viral infections and exposition to low doses of lipopolysaccharide (LPS) strongly increase the risk of disease inception. Interestingly, these two particular risk factors both induce a strong recruitment of neutrophils into the lung. Recently, scientists highlighted the ability of neutrophils to form neutrophils extracellular traps (NETs) composed of a network of extracellular DNA associated to anti-microbial peptides. NETs release (or NETosis) is an important component in organism defence against pathogen invasion but has also been identified as initiator of pathophysiological conditions like erythematous systemic lupus, gout and diabetes. In this study, we investigated the role of NETs as potential asthma inducers in specific pro-Th2 environmental risk factors like respiratory viral infections and low LPS doses exposures (also known as hygiene hypothesis). First, we assessed the correlation between respiratory viral infection or low LPS exposure and NETosis using western blot and confocal microscopy analysis. An influenza A infection induced a strong NETs release between day three and seven after viral inoculation whereas exposition to low (100 ng LPS) but not to high (10 µg LPS) LPS doses also promoted NETosis within 24 hours following the exposition. Then we developed two mouse models, a virus-induced asthma model and a model of asthma promoted by exposition to low LPS doses. In these models, only previously infected mice or mice exposed to low LPS doses displayed all the characteristics of allergic asthma following sensitization and challenge to house dust mite (HDM). The role of NETs in asthma onset was then demonstrated using three NETosis inhibitors (DNAse, Cl-amidine and inhibitor of neutrophil elastase) in our models as infected or low LPS doses exposed mice exhibited strong decreased of all key asthma features when treated with NETs inhibitors compared to non-treated mice. Finally, to address how NETs could lead to a TH2 immune response, we analysed by flow cytometry the distinct subpopulations of lung dendritic cells (DCs) in our two mice models. We observed, during the NETs release phase, a recruitment of monocytic derived DCs (moDCs). In conclusion, we have demonstrated an unexpected role for NETs in asthma onset by recruiting lung moDCs. [less ▲]

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See detailRelease of Neutrophils Extracellular Traps as a main trigger for asthma onset
Radermecker, Coraline ULiege; Sabatel, Catherine ULiege; Toussaint, Marie et al

Conference (2017, January 24)

Allergic asthma is an important Th2 associated immunopathology. Even if the pathology of the disease is well described, its etiology is still largely unknown. Nevertheless, some environmental factors like ... [more ▼]

Allergic asthma is an important Th2 associated immunopathology. Even if the pathology of the disease is well described, its etiology is still largely unknown. Nevertheless, some environmental factors like viral infections and exposition to low doses of lipopolysaccharide (LPS) strongly increase the risk of disease inception. Interestingly, these two particular risk factors both induce a strong recruitment of neutrophils into the lung. Recently, scientists highlighted the ability of neutrophils to form neutrophils extracellular traps (NETs) composed of a network of extracellular DNA associated to anti-microbial peptides. NETs release (or NETosis) is an important component in organism defence against pathogen invasion but has also been identified as initiator of pathophysiological conditions like erythematous systemic lupus, gout and diabetes. In this study, we investigated the role of NETs as potential asthma inducers in specific pro-Th2 environmental risk factors like respiratory viral infections and low LPS doses exposures (also known as hygiene hypothesis). First, we assessed the correlation between respiratory viral infection or low LPS exposure and NETosis using western blot and confocal microscopy analysis. An influenza A infection induced a strong NETs release between day three and seven after viral inoculation whereas exposition to low (100 ng LPS) but not to high (10 µg LPS) LPS doses also promoted NETosis within 24 hours following the exposition. Then we developed two mouse models, a virus-induced asthma model and a model of asthma promoted by exposition to low LPS doses. In these models, only previously infected mice or mice exposed to low LPS doses displayed all the characteristics of allergic asthma following sensitization and challenge to house dust mite (HDM). The role of NETs in asthma onset was then demonstrated using three NETosis inhibitors (DNAse, Cl-amidine and inhibitor of neutrophil elastase) in our models as infected or low LPS doses exposed mice exhibited strong decreased of all key asthma features when treated with NETs inhibitors compared to non-treated mice. Finally, to address how NETs could lead to a TH2 immune response, we analysed by flow cytometry the distinct subpopulations of lung dendritic cells (DCs) in our two mice models. We observed, during the NETs release phase, a recruitment of monocytic derived DCs (moDCs). In conclusion, we have demonstrated an unexpected role for NETs in asthma onset by recruiting lung moDCs. [less ▲]

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See detailHost DNA released by NETosis promotes rhinovirus-induced type-2 allergic asthma exacerbation.
Toussaint, Marie; Jackson, David J.; Swieboda, Dawid et al

in Nature Medicine (2017), 23

Respiratory viral infections represent the most common cause of allergic asthma exacerbations. Amplification of the type-2 immune response is strongly implicated in asthma exacerbation, but how virus ... [more ▼]

Respiratory viral infections represent the most common cause of allergic asthma exacerbations. Amplification of the type-2 immune response is strongly implicated in asthma exacerbation, but how virus infection boosts type-2 responses is poorly understood. We report a significant correlation between the release of host double-stranded DNA (dsDNA) following rhinovirus infection and the exacerbation of type-2 allergic inflammation in humans. In a mouse model of allergic airway hypersensitivity, we show that rhinovirus infection triggers dsDNA release associated with the formation of neutrophil extracellular traps (NETs), known as NETosis. We further demonstrate that inhibiting NETosis by blocking neutrophil elastase or by degrading NETs with DNase protects mice from type-2 immunopathology. Furthermore, the injection of mouse genomic DNA alone is sufficient to recapitulate many features of rhinovirus-induced type-2 immune responses and asthma pathology. Thus, NETosis and its associated extracellular dsDNA contribute to the pathogenesis and may represent potential therapeutic targets of rhinovirus-induced asthma exacerbations. [less ▲]

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See detailNeutrophil myeloperoxidase diminishes the toxic effects and mortality induced by lipopolysaccharide.
Reber, Laurent L.; Gillis, Caitlin M.; Starkl, Philipp et al

in Journal of Experimental Medicine (2017), 214(5), 1249-1258

Neutrophils have crucial antimicrobial functions but are also thought to contribute to tissue injury upon exposure to bacterial products, such as lipopolysaccharide (LPS). To study the role of neutrophils ... [more ▼]

Neutrophils have crucial antimicrobial functions but are also thought to contribute to tissue injury upon exposure to bacterial products, such as lipopolysaccharide (LPS). To study the role of neutrophils in LPS-induced endotoxemia, we developed a new mouse model, PMNDTR mice, in which injection of diphtheria toxin induces selective neutrophil ablation. Using this model, we found, surprisingly, that neutrophils serve to protect the host from LPS-induced lethal inflammation. This protective role was observed in conventional and germ-free animal facilities, indicating that it does not depend on a particular microbiological environment. Blockade or genetic deletion of myeloperoxidase (MPO), a key neutrophil enzyme, significantly increased mortality after LPS challenge, and adoptive transfer experiments confirmed that neutrophil-derived MPO contributes importantly to protection from endotoxemia. Our findings imply that, in addition to their well-established antimicrobial properties, neutrophils can contribute to optimal host protection by limiting the extent of endotoxin-induced inflammation in an MPO-dependent manner. [less ▲]

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See detailExposure to Bacterial CpG DNA Protects from Airway Allergic Inflammation by Expanding Regulatory Lung Interstitial Macrophages.
Sabatel, Catherine ULiege; Radermecker, Coraline ULiege; Fievez, Laurence ULiege et al

in Immunity (2017), 46(3), 457-473

Living in a microbe-rich environment reduces the risk of developing asthma. Exposure of humans or mice to unmethylated CpG DNA (CpG) from bacteria reproduces these protective effects, suggesting a major ... [more ▼]

Living in a microbe-rich environment reduces the risk of developing asthma. Exposure of humans or mice to unmethylated CpG DNA (CpG) from bacteria reproduces these protective effects, suggesting a major contribution of CpG to microbe-induced asthma resistance. However, how CpG confers protection remains elusive. We found that exposure to CpG expanded regulatory lung interstitial macrophages (IMs) from monocytes infiltrating the lung or mobilized from the spleen. Trafficking of IM precursors to the lung was independent of CCR2, a chemokine receptor required for monocyte mobilization from the bone marrow. Using a mouse model of allergic airway inflammation, we found that adoptive transfer of IMs isolated from CpG-treated mice recapitulated the protective effects of CpG when administered before allergen sensitization or challenge. IM-mediated protection was dependent on IL-10, given that Il10-/- CpG-induced IMs lacked regulatory effects. Thus, the expansion of regulatory lung IMs upon exposure to CpG might underlie the reduced risk of asthma development associated with a microbe-rich environment. [less ▲]

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See detailEpithelial Rab guanine nucleotide exchange factor 1 (Rabgef1) deficiency increases susceptibility to DSS-induced intestinal inflammation in mice
El Abbas, Sophie ULiege; Beguin, C; Mesnil, Claire ULiege et al

in Proceedings: 3rd FARAH-DAY (2016, October 21)

Rab guanine nucleotide exchange factor (GEF)1 (Rabgef1) is a guanine nucleotide exchange factor for the endocytic GTPase Rab5, and also exhibits E3 ubiquitin ligase activity in vitro. In vivo functions of ... [more ▼]

Rab guanine nucleotide exchange factor (GEF)1 (Rabgef1) is a guanine nucleotide exchange factor for the endocytic GTPase Rab5, and also exhibits E3 ubiquitin ligase activity in vitro. In vivo functions of Rabgef1 remain largely unknown, but Rabgef1 is critical for health, as globally Rabgef1-deficient mice exhibit perinatal mortality and those surviving to adulthood spontaneously develop severe skin inflammation.This protein is highly expressed in murine intestinal epithelial cells (IECs). Objective: The aim of this study is to clarify the role of Rabgef1 in murine IECs Materials and methods: We performed conditional deletion of Rabgef1 using the cre-lox system to obtain mice lacking Rabgef1 specifically in IECs (Rabgef1IEC-KO). Results: Rabgef1IEC-KO mice did not develop spontaneous intestinal abnormalities but showed an increased susceptibility to inflammation in dextran sodium sulfate (DSS)-induced col itis model. Indeed, compared to littermate controls, mice lacking Rabgef1 in IECs exhibited shorter and highly inflamed colons and higher inflammatory scores in histopathological examination of colons, suggesting that Rabgef1 expression regulates IEC function and is critical in limiting DSS induced inflammation and damage. In addition, we also showed that mRNA expression of pro-inflammatory cytokines, such as Il1b and Tnfa, was upregulated in IECs isolated from Rabgef1IEC-KO mice compared to the ones isolated from littermate controls. Conclusion: Taken together, these results suggest that Rabgef1 acts as a regulator of intestinal homeostasis, and that dysregulated Rabgef1 expression could contribute to intestinal barrier dysfunction in inflammatory conditions of the gut. [less ▲]

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See detailLung resident eosinophils represent a distinct cell subset with homeostatic functions
Mesnil, Claire ULiege; Raulier, Stéfanie ULiege; Paulissen, Geneviève et al

Conference (2016, October 21)

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See detailCpG-DNA expand immunosuppressive interstitial macrophages from Ly6c+ local precursors
Sabatel, Catherine ULiege; Radermecker, Coraline ULiege; Fievez, Laurence ULiege et al

in Proceeding of Cell Symposia: 100 years of phagocytes (2016, September)

Detailed reference viewed: 27 (3 ULiège)
See detailEpithelial Rab guanine nucleotide exchange factor 1 (Rabgef1) deficiency increases susceptibility to DSS-induced intestinal inflammation in mice
El Abbas, Sophie ULiege; Beguin, C; Mesnil, Claire ULiege et al

Poster (2016, May 27)

Rab guanine nucleotide exchange factor (GEF)1 (Rabgef1) is a guanine nucleotide exchange factor for the endocytic GTPase Rab5, and also exhibits E3 ubiquitin ligase activity in vitro. In vivo functions of ... [more ▼]

Rab guanine nucleotide exchange factor (GEF)1 (Rabgef1) is a guanine nucleotide exchange factor for the endocytic GTPase Rab5, and also exhibits E3 ubiquitin ligase activity in vitro. In vivo functions of Rabgef1 remain largely unknown, but Rabgef1 is critical for health, as globally Rabgef1-deficient mice exhibit perinatal mortality and those surviving to adulthood spontaneously develop severe skin inflammation. In the mouse gut, we found that Rabgef1 is highly expressed in intestinal epithelial cells (IECs). We performed conditional deletion of Rabgef1 using the cre-lox system to obtain mice lacking Rabgef1 specifically in IECs (Rabgef1IEC-KO). These mice did not develop spontaneous intestinal abnormalities but showed an increased susceptibility to inflammation in dextran sodium sulfate (DSS)-induced colitis model. Indeed, compared to littermate controls, mice lacking Rabgef1 in IECs exhibited shorter and highly inflamed colons and higher inflammatory scores in histopathological examination of colons, suggesting that Rabgef1 expression regulates IEC function and is critical in limiting DSS induced inflammation and damage. In addition, we also showed that mRNA expression of pro-inflammatory cytokines, such as Il1b and Tnfa, was upregulated in IECs isolated from Rabgef1IEC-KO mice compared to the ones isolated from littermate controls. Taken together, these results suggest that Rabgef1 acts as a regulator of intestinal homeostasis, and that dysregulated Rabgef1 expression could contribute to intestinal barrier dysfunction in inflammatory conditions of the gut. [less ▲]

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See detailKeratinocyte RabGEF1 maintains skin homeostasis in vivo.
Marichal, Thomas ULiege

Conference (2016, April 22)

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See detailGuanine nucleotide exchange factor RABGEF1 regulates keratinocyte-intrinsic signaling to maintain skin homeostasis.
Marichal, Thomas ULiege; Gaudenzio, Nicolas; El Abbas, Sophie ULiege et al

in Journal of Clinical Investigation (2016), 126(12), 4497-4515

Epidermal keratinocytes form a structural and immune barrier that is essential for skin homeostasis. However, the mechanisms that regulate epidermal barrier function are incompletely understood. Here we ... [more ▼]

Epidermal keratinocytes form a structural and immune barrier that is essential for skin homeostasis. However, the mechanisms that regulate epidermal barrier function are incompletely understood. Here we have found that keratinocyte-specific deletion of the gene encoding RAB guanine nucleotide exchange factor 1 (RABGEF1, also known as RABEX-5) severely impairs epidermal barrier function in mice and induces an allergic cutaneous and systemic phenotype. RABGEF1-deficient keratinocytes exhibited aberrant activation of the intrinsic IL-1R/MYD88/NF-kappaB signaling pathway and MYD88-dependent abnormalities in expression of structural proteins that contribute to skin barrier function. Moreover, ablation of MYD88 signaling in RABGEF1-deficient keratinocytes or deletion of Il1r1 restored skin homeostasis and prevented development of skin inflammation. We further demonstrated that epidermal RABGEF1 expression is reduced in skin lesions of humans diagnosed with either atopic dermatitis or allergic contact dermatitis as well as in an inducible mouse model of allergic dermatitis. Our findings reveal a key role for RABGEF1 in dampening keratinocyte-intrinsic MYD88 signaling and sustaining epidermal barrier function in mice, and suggest that dysregulation of RABGEF1 expression may contribute to epidermal barrier dysfunction in allergic skin disorders in mice and humans. Thus, RABGEF1-mediated regulation of IL-1R/MYD88 signaling might represent a potential therapeutic target. [less ▲]

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See detailLung-resident eosinophils represent a distinct regulatory eosinophil subset
Mesnil, Claire ULiege; Raulier, Stéfanie ULiege; Paulissen, G et al

in Journal of Clinical Investigation (2016), 126(9), 3275-3295

Increases in eosinophil numbers are associated with infection and allergic diseases, including asthma, but there is also evidence that eosinophils contribute to homeostatic immune processes. In mice, the ... [more ▼]

Increases in eosinophil numbers are associated with infection and allergic diseases, including asthma, but there is also evidence that eosinophils contribute to homeostatic immune processes. In mice, the normal lung contains resident eosinophils (rEos), but their function has not been characterized. Here, we have reported that steady-state pulmonary rEos are IL-5–independent parenchymal Siglec-FintCD62L+CD101lo cells with a ring-shaped nucleus. During house dust mite–induced airway allergy, rEos features remained unchanged, and rEos were accompanied by recruited inflammatory eosinophils (iEos), which were defined as IL-5–dependent peribronchial Siglec-FhiCD62L–CD101hi cells with a segmented nucleus. Gene expression analyses revealed a more regulatory profile for rEos than for iEos, and correspondingly, mice lacking lung rEos showed an increase in Th2 cell responses to inhaled allergens. Such elevation of Th2 responses was linked to the ability of rEos, but not iEos, to inhibit the maturation, and therefore the pro-Th2 function, of allergen-loaded DCs. Finally, we determined that the parenchymal rEos found in nonasthmatic human lungs (Siglec-8+CD62L+IL-3Rlo cells) were phenotypically distinct from the iEos isolated from the sputa of eosinophilic asthmatic patients (Siglec-8+CD62LloIL-3Rhi cells), suggesting that our findings in mice are relevant to humans. In conclusion, our data define lung rEos as a distinct eosinophil subset with key homeostatic functions. [less ▲]

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See detailDifferent activation signals induce distinct mast cell degranulation strategies.
Gaudenzio, Nicolas; Sibilano, Riccardo; Marichal, Thomas ULiege et al

in Journal of Clinical Investigation (2016), 126(10), 3981-3998

Mast cells (MCs) influence intercellular communication during inflammation by secreting cytoplasmic granules that contain diverse mediators. Here, we have demonstrated that MCs decode different activation ... [more ▼]

Mast cells (MCs) influence intercellular communication during inflammation by secreting cytoplasmic granules that contain diverse mediators. Here, we have demonstrated that MCs decode different activation stimuli into spatially and temporally distinct patterns of granule secretion. Certain signals, including substance P, the complement anaphylatoxins C3a and C5a, and endothelin 1, induced human MCs rapidly to secrete small and relatively spherical granule structures, a pattern consistent with the secretion of individual granules. Conversely, activating MCs with anti-IgE increased the time partition between signaling and secretion, which was associated with a period of sustained elevation of intracellular calcium and formation of larger and more heterogeneously shaped granule structures that underwent prolonged exteriorization. Pharmacological inhibition of IKK-beta during IgE-dependent stimulation strongly reduced the time partition between signaling and secretion, inhibited SNAP23/STX4 complex formation, and switched the degranulation pattern into one that resembled degranulation induced by substance P. IgE-dependent and substance P-dependent activation in vivo also induced different patterns of mouse MC degranulation that were associated with distinct local and systemic pathophysiological responses. These findings show that cytoplasmic granule secretion from MCs that occurs in response to different activating stimuli can exhibit distinct dynamics and features that are associated with distinct patterns of MC-dependent inflammation. [less ▲]

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See detailPathways of immediate hypothermia and leukocyte infiltration in an adjuvant-free mouse model of anaphylaxis.
Balbino, Bianca; Sibilano, Riccardo; Starkl, Philipp et al

in Journal of Allergy and Clinical Immunology (The) (2016)

BACKGROUND: Conflicting results have been obtained regarding the roles of Fc receptors and effector cells in models of active systemic anaphylaxis (ASA). In part, this might reflect the choice of adjuvant ... [more ▼]

BACKGROUND: Conflicting results have been obtained regarding the roles of Fc receptors and effector cells in models of active systemic anaphylaxis (ASA). In part, this might reflect the choice of adjuvant used during sensitization because various adjuvants might differentially influence the production of particular antibody isotypes. OBJECTIVE: We developed an "adjuvant-free" mouse model of ASA and assessed the contributions of components of the "classical" and "alternative" pathways in this model. METHODS: Mice were sensitized intraperitoneally with ovalbumin at weekly intervals for 6 weeks and challenged intraperitoneally with ovalbumin 2 weeks later. RESULTS: Wild-type animals had immediate hypothermia and late-phase intraperitoneal inflammation in this model. These features were reduced in mice lacking the IgE receptor FcepsilonRI, the IgG receptor FcgammaRIII or the common gamma-chain FcRgamma. FcgammaRIV blockade resulted in a partial reduction of inflammation without any effect on hypothermia. Depletion of monocytes/macrophages with clodronate liposomes significantly reduced the hypothermia response. By contrast, depletion of neutrophils or basophils had no significant effects in this ASA model. Both the hypothermia and inflammation were dependent on platelet-activating factor and histamine and were reduced in 2 types of mast cell (MC)-deficient mice. Finally, engraftment of MC-deficient mice with bone marrow-derived cultured MCs significantly exacerbated the hypothermia response and restored inflammation to levels similar to those observed in wild-type mice. CONCLUSION: Components of the classical and alternative pathways contribute to anaphylaxis in this adjuvant-free model, with key roles for MCs and monocytes/macrophages. [less ▲]

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See detailInterferon response factor-3 promotes the pro-Th2 activity of mouse myeloid CD11b+ dendritic cells
Janss, Thibaut ULiege; Mesnil, Claire ULiege; Pirottin, Dimitri ULiege et al

in European Journal of Immunology (2016), 46

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See detailRole of double-stranded DNA in allergic airway inflammation.
Marichal, Thomas ULiege

Conference (2016)

Detailed reference viewed: 4 (1 ULiège)