6 results on '"Heslan, M."'
Search Results
2. IL-22BP is produced by eosinophils in human gut and blocks IL-22 protective actions during colitis
- Author
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Martin, J C, primary, Bériou, G, additional, Heslan, M, additional, Bossard, C, additional, Jarry, A, additional, Abidi, A, additional, Hulin, P, additional, Ménoret, S, additional, Thinard, R, additional, Anegon, I, additional, Jacqueline, C, additional, Lardeux, B, additional, Halary, F, additional, Renauld, J-C, additional, Bourreille, A, additional, and Josien, R, additional
- Published
- 2016
- Full Text
- View/download PDF
3. Interleukin-22 level is negatively correlated with neutrophil recruitment in the lungs in a Pseudomonas aeruginosa pneumonia model.
- Author
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Broquet A, Jacqueline C, Davieau M, Besbes A, Roquilly A, Martin J, Caillon J, Dumoutier L, Renauld JC, Heslan M, Josien R, and Asehnoune K
- Subjects
- Animals, Disease Models, Animal, Mice, Interleukin-22, Interleukins analysis, Lung pathology, Neutrophil Infiltration, Pneumonia, Bacterial pathology, Pseudomonas Infections pathology, Receptors, Interleukin analysis
- Abstract
Pseudomonas aeruginosa is a major threat for immune-compromised patients. Bacterial pneumonia can induce uncontrolled and massive neutrophil recruitment ultimately leading to acute respiratory distress syndrome and epithelium damage. Interleukin-22 plays a central role in the protection of the epithelium. In this study, we aimed to evaluate the role of interleukin-22 and its soluble receptor IL-22BP in an acute Pseudomonas aeruginosa pneumonia model in mice. In this model, we noted a transient increase of IL-22 during Pseudomonas aeruginosa challenge. Using an antibody-based approach, we demonstrated that IL-22 neutralisation led to increased susceptibility to infection and to lung damage correlated with an increase in neutrophil accumulation in the lungs. On the contrary, rIL-22 administration or IL-22BP neutralisation led to a decrease in mouse susceptibility and lung damage associated with a decrease in neutrophil accumulation. This study demonstrated that the IL-22/IL-22BP system plays a major role during Pseudomonas aeruginosa pneumonia by moderating neutrophil accumulation in the lungs that ultimately leads to epithelium protection.
- Published
- 2017
- Full Text
- View/download PDF
4. Functional Langerinhigh-Expressing Langerhans-like Cells Can Arise from CD14highCD16- Human Blood Monocytes in Serum-Free Condition.
- Author
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Picarda G, Chéneau C, Humbert JM, Bériou G, Pilet P, Martin J, Duteille F, Perrot P, Bellier-Waast F, Heslan M, Haspot F, Guillon F, Josien R, and Halary FA
- Subjects
- Antigens, Neoplasm metabolism, Cell Adhesion Molecules metabolism, Cell Differentiation, Cells, Cultured, Humans, Isoantigens immunology, Lipopolysaccharide Receptors metabolism, Lymphocyte Activation, Proto-Oncogene Proteins metabolism, Receptor Protein-Tyrosine Kinases metabolism, Receptors, IgG metabolism, Self Tolerance, Ultraviolet Rays, Axl Receptor Tyrosine Kinase, Blood Cells physiology, Granulocyte-Macrophage Colony-Stimulating Factor metabolism, Keratinocytes physiology, Langerhans Cells immunology, Monocytes physiology, T-Lymphocytes immunology, Transforming Growth Factor beta1 metabolism
- Abstract
Langerhans cells (LCs) are epithelial APCs that sense danger signals and in turn trigger specific immune responses. In steady-state, they participate in the maintenance of peripheral tolerance to self-antigens whereas under inflammation LCs efficiently trigger immune responses in secondary lymphoid organs. It has been demonstrated in mice that LC-deprived epithelia are rapidly replenished by short half-life langerin-expressing monocyte-derived LCs (MDLCs). These surrogate LCs are thought to be progressively replaced by langerin(high) LCs arising from self-renewing epithelial precursors of hematopoietic origin. How LCs arise from blood monocytes is not fully understood. Hence, we sought to characterize key factors that induce differentiation of langerin(high)-expressing monocyte-derived Langerhans-like cells. We identified GM-CSF and TGF-β1 as key cytokines to generate langerin(high)-expressing cells but only in serum-free conditions. These cells were shown to express the LC-specific TROP-2 and Axl surface markers and contained Birbeck granules. Surprisingly, E-cadherin was not spontaneously expressed by these cells but required a direct contact with keratinocytes to be stably induced. MDLCs induced stronger allogeneic T cell proliferations but released low amounts of inflammatory cytokines upon TLR stimulation compared with donor-paired monocyte-derived dendritic cells. Immature langerin(high) MDLCs were responsive to MIP-3β/CCL20 and CTAC/CCL27 chemokine stimulations. Finally, we demonstrated that those cells behaved as bona fide LCs when inserted in a three-dimensional rebuilt epithelium by becoming activated upon TLR or UV light stimulations. Collectively, these results prompt us to propose these langerin(high) MDLCs as a relevant model to address LC biology-related questions., (Copyright © 2016 by The American Association of Immunologists, Inc.)
- Published
- 2016
- Full Text
- View/download PDF
5. Regulatory B Cells with a Partial Defect in CD40 Signaling and Overexpressing Granzyme B Transfer Allograft Tolerance in Rodents.
- Author
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Durand J, Huchet V, Merieau E, Usal C, Chesneau M, Remy S, Heslan M, Anegon I, Cuturi MC, Brouard S, and Chiffoleau E
- Subjects
- Allografts, Animals, Antigens, CD immunology, Cytokines immunology, Isoantigens immunology, Male, Rats, T-Lymphocytes, Regulatory immunology, B-Lymphocytes, Regulatory immunology, CD40 Antigens immunology, Granzymes immunology, Heart Transplantation, Plasma Cells immunology, Signal Transduction immunology, Transplantation Tolerance
- Abstract
Emerging knowledge regarding B cells in organ transplantation has demonstrated that these cells can no longer be taken as mere generators of deleterious Abs but can also act as beneficial players. We previously demonstrated in a rat model of cardiac allograft tolerance induced by short-term immunosuppression an accumulation in the blood of B cells overexpressing inhibitory molecules, a phenotype also observed in the blood of patients that spontaneously develop graft tolerance. In this study, we demonstrated the presence in the spleen of regulatory B cells enriched in the CD24(int)CD38(+)CD27(+)IgD(-)IgM(+/low) subpopulation, which are able to transfer donor-specific tolerance via IL-10 and TGF-β1-dependent mechanisms and to suppress in vitro TNF-α secretion. Following anti-CD40 stimulation, IgD(-)IgM(+/low) B cells were blocked in their plasma cell differentiation pathway, maintained high expression of the inhibitory molecules CD23 and Bank1, and upregulated Granzyme B and Irf4, two molecules described as highly expressed by regulatory B cells. Interestingly, these B cells recognized specifically a dominant donor Ag, suggesting restricted specificity that could lead to a particular B cell response. Regulatory B cells were not required for induction of tolerance and appeared following Foxp3(+)CD4(+)CD25(+) regulatory T cells, suggesting cooperation with regulatory T cells for their expansion. Nevertheless, following transfer to new recipients, these B cells migrated to the allograft, kept their regulatory profile, and promoted local accumulation of Foxp3(+)CD4(+)CD25(+) regulatory T cells. Mechanisms of regulatory B cells and their cell therapy potential are important to decipher in experimental models to pave the way for future developments in the clinic., (Copyright © 2015 by The American Association of Immunologists, Inc.)
- Published
- 2015
- Full Text
- View/download PDF
6. Receptor activating NF-κB ligand (RANKL) is a constitutive intracellular protein in resting human basophils and is strongly induced on their surface by interleukin 3.
- Author
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Poli C, Martin JC, Braudeau C, Bériou G, Hémont C, Charrier C, Guérin S, Heslan M, and Josien R
- Subjects
- Cell Communication, Cell Differentiation, Cells, Cultured, Humans, Interleukin-3 immunology, Protein Transport immunology, RANK Ligand genetics, Up-Regulation immunology, Basophils immunology, Bone Resorption immunology, Cell Membrane metabolism, Dendritic Cells immunology, Intracellular Space metabolism, Osteoclasts physiology, RANK Ligand metabolism
- Abstract
Receptor activating NF-κB ligand (RANKL) is a member of the TNF superfamily that plays a pivotal role in bone homeostasis as being the major osteoclastogenesis factor. RANKL also has pleiotropic effects in the immune system in which it is expressed by activated T and B cells and some innate lymphoid cells. RANKL-RANK interactions mediate lymph node organogenesis and immunoregulatory functions in autoimmune disease and carcinogenesis as well as cross talk between the immune system and bone. In this study, we show that basophils were the strongest RANKL mRNA-expressing cells amongst major leukocyte subsets in human blood. RANKL was preformed as an intracellular protein in resting basophils and was rapidly and strongly expressed on their surface upon stimulation with IL-3, but not other stimuli. This expression was stable for at least 6 days. Activated basophils could also release soluble RANKL in small quantities upon interaction with DCs or monocytes. In the blood, basophils were the sole cells to express membrane RANKL in response to IL-3. This study indicates that basophils should be considered as new players in the pleiotropic and complex RANKL-RANK interaction system and suggests a role for RANKL in the interaction between basophils and immune cells in inflammatory allergic tissues and secondary lymphoid organs., (Copyright © 2014 Elsevier GmbH. All rights reserved.)
- Published
- 2015
- Full Text
- View/download PDF
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