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Article ; Online: Correction to: Comment on "ILC1 drive intestinal epithelial and matrix remodeling".

Hariss, Fatima / Meresse, Bertrand

2022 Volume 15, Issue 3, Page(s) 530

Language	English
Publishing date	2022-03-31
Publishing country	United States
Document type	Published Erratum
ZDB-ID	2411370-0
ISSN	1935-3456 ; 1933-0219
ISSN (online)	1935-3456
ISSN	1933-0219
DOI	10.1038/s41385-022-00508-9
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Zs.A 6796: Show issues

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Article ; Online: Comment on "ILC1 drive intestinal epithelial and matrix remodeling".

Hariss, Fatima / Meresse, Bertrand

Mucosal immunology

2021 Volume 14, Issue 2, Page(s) 279–281

MeSH term(s)	Intestines ; Killer Cells, Natural
Language	English
Publishing date	2021-02-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2411370-0
ISSN	1935-3456 ; 1933-0219
ISSN (online)	1935-3456
ISSN	1933-0219
DOI	10.1038/s41385-020-00360-9
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Zs.A 6796: Show issues

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Article ; Online: Cytotoxic innate intraepithelial lymphocytes control early stages of

Hariss, Fatima / Delbeke, Marie / Guyot, Karine / Zarnitzky, Pauline / Ezzedine, Mohamad / Certad, Gabriela / Meresse, Bertrand

Frontiers in immunology

2023 Volume 14, Page(s) 1229406

Abstract: Background: Intraepithelial lymphocytes (IELs) are the first immune cells to contact and fight intestinal pathogens such as : Methods: To better define functions of innate IELs in cryptosporidiosis, we developed a co-culture model with innate IELs ... ...

Abstract	Background: Intraepithelial lymphocytes (IELs) are the first immune cells to contact and fight intestinal pathogens such as Methods: To better define functions of innate IELs in cryptosporidiosis, we developed a co-culture model with innate IELs isolated from Results: Thanks to this original model, we demonstrated that innate IELs control parasite proliferation. We further showed that although innate IELs secrete IFN-γ in response to Conclusion: Based on these data we conclude that innate IELs, most likely T-cell-like innate IELs, provide a rapid protection against
MeSH term(s)	Animals ; Mice ; Cryptosporidiosis ; Cryptosporidium ; Granzymes ; Immunity, Innate ; Intraepithelial Lymphocytes ; Lymphocytes ; Antineoplastic Agents
Chemical Substances	Granzymes (EC 3.4.21.-) ; Antineoplastic Agents
Language	English
Publishing date	2023-09-06
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1229406
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Article ; Online: Targeting CCR4 with mogamulizumab in refractory CD3-CD4

Ledoult, Emmanuel / Groh, Matthieu / Meresse, Bertrand / Dubois, Romain / Trauet, Jacques / Toussaint, Elise / Delbeke, Marie / Hachulla, Eric / Terriou, Louis / De Masson, Adèle / Vasseur, Michele / Labalette, Myriam / Launay, David / Kahn, Jean-Emmanuel / Lefevre, Guillaume

Haematologica

2024

Abstract: Not available. ...

Abstract	Not available.
Language	English
Publishing date	2024-02-08
Publishing country	Italy
Document type	Journal Article
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2023.284429
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Article ; Online: Real-time glioblastoma tumor microenvironment assessment by SpiderMass for improved patient management.

Zirem, Yanis / Ledoux, Léa / Roussel, Lucas / Maurage, Claude Alain / Tirilly, Pierre / Le Rhun, Émilie / Meresse, Bertrand / Yagnik, Gargey / Lim, Mark J / Rothschild, Kenneth J / Duhamel, Marie / Salzet, Michel / Fournier, Isabelle

Cell reports. Medicine

2024 Volume 5, Issue 4, Page(s) 101482

Abstract: Glioblastoma is a highly heterogeneous and infiltrative form of brain cancer associated with a poor outcome and limited therapeutic effectiveness. The extent of the surgery is related to survival. Reaching an accurate diagnosis and prognosis assessment ... ...

Abstract	Glioblastoma is a highly heterogeneous and infiltrative form of brain cancer associated with a poor outcome and limited therapeutic effectiveness. The extent of the surgery is related to survival. Reaching an accurate diagnosis and prognosis assessment by the time of the initial surgery is therefore paramount in the management of glioblastoma. To this end, we are studying the performance of SpiderMass, an ambient ionization mass spectrometry technology that can be used in vivo without invasiveness, coupled to our recently established artificial intelligence pipeline. We demonstrate that we can both stratify isocitrate dehydrogenase (IDH)-wild-type glioblastoma patients into molecular sub-groups and achieve an accurate diagnosis with over 90% accuracy after cross-validation. Interestingly, the developed method offers the same accuracy for prognosis. In addition, we are testing the potential of an immunoscoring strategy based on SpiderMass fingerprints, showing the association between prognosis and immune cell infiltration, to predict patient outcome.
MeSH term(s)	Humans ; Glioblastoma ; Artificial Intelligence ; Tumor Microenvironment ; Brain Neoplasms/diagnosis ; Prognosis
Language	English
Publishing date	2024-03-28
Publishing country	United States
Document type	Journal Article
ISSN	2666-3791
ISSN (online)	2666-3791
DOI	10.1016/j.xcrm.2024.101482
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Article ; Online: Coeliac disease &gluten sensitivity: Epithelial stress enters the dance in coeliac disease.

Cerf-Bensussan, Nadine / Meresse, Bertrand

Nature reviews. Gastroenterology & hepatology

2015 Volume 12, Issue 9, Page(s) 491–492

MeSH term(s)	Adaptive Immunity ; Celiac Disease/immunology ; Cell Communication ; Epithelial Cells/immunology ; Humans ; Intestinal Mucosa/immunology ; Intestine, Small/immunology ; Stress, Physiological ; T-Lymphocytes, Cytotoxic/immunology
Language	English
Publishing date	2015-09
Publishing country	England
Document type	Comment ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2493722-8
ISSN	1759-5053 ; 1759-5045
ISSN (online)	1759-5053
ISSN	1759-5045
DOI	10.1038/nrgastro.2015.120
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Zs.A 6020: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 97: Show issues

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Article ; Online: Innate T cell responses in human gut.

Meresse, Bertrand / Cerf-Bensussan, Nadine

Seminars in immunology

2009 Volume 21, Issue 3, Page(s) 121–129

Abstract: One arm of the gut-associated immune system is represented by a vast collection of T lymphocytes which participate in the subtle interplay between innate and adaptive immune mechanisms and maintain homeostasis at the main body external surface. Mounting ... ...

Abstract	One arm of the gut-associated immune system is represented by a vast collection of T lymphocytes which participate in the subtle interplay between innate and adaptive immune mechanisms and maintain homeostasis at the main body external surface. Mounting data are providing exciting new insight into the innate-like mechanisms which enable intestinal T cells to rapidly sense local conditions and which broaden the spectrum of their functions and regulation at this strategic location. Herein we discuss how innate-like T cell recognition by unconventional T cell subsets and expression of innate NK receptors might modulate immune T cell responses in the human normal or diseased intestine.
MeSH term(s)	Animals ; Humans ; Immunity, Cellular ; Immunity, Innate ; Immunity, Mucosal ; Intestinal Mucosa/immunology ; Intestinal Mucosa/metabolism ; Intestinal Mucosa/pathology ; Intestines/immunology ; Mice ; NK Cell Lectin-Like Receptor Subfamily D/immunology ; NK Cell Lectin-Like Receptor Subfamily D/metabolism ; NK Cell Lectin-Like Receptor Subfamily K/immunology ; NK Cell Lectin-Like Receptor Subfamily K/metabolism ; Natural Killer T-Cells/immunology ; Natural Killer T-Cells/metabolism ; Natural Killer T-Cells/pathology ; Receptors, Antigen, T-Cell, gamma-delta/metabolism
Chemical Substances	NK Cell Lectin-Like Receptor Subfamily D ; NK Cell Lectin-Like Receptor Subfamily K ; Receptors, Antigen, T-Cell, gamma-delta
Language	English
Publishing date	2009-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1018141-6
ISSN	1096-3618 ; 1044-5323
ISSN (online)	1096-3618
ISSN	1044-5323
DOI	10.1016/j.smim.2009.01.002
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Zs.A 2843: Show issues

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Article ; Online: Interleukin-15, a master piece in the immunological jigsaw of celiac disease.

Meresse, Bertrand / Korneychuk, Natalia / Malamut, Georgia / Cerf-Bensussan, Nadine

Digestive diseases (Basel, Switzerland)

2015 Volume 33, Issue 2, Page(s) 122–130

Abstract: Background: The immune response causing celiac disease (CD) depends on the activation of intestinal CD4+ T cells by gluten-derived peptides presented by HLA-DQ2 or HLA-DQ8 molecules, the main genetic risk factor. However, additional factors are ... ...

Abstract	Background: The immune response causing celiac disease (CD) depends on the activation of intestinal CD4+ T cells by gluten-derived peptides presented by HLA-DQ2 or HLA-DQ8 molecules, the main genetic risk factor. However, additional factors are necessary to impair immune tolerance to dietary gluten, to stimulate intraepithelial lymphocytes (IEL) and to induce intestinal damage. Key messages: Current data point to a central role of interleukin-15 (IL-15). In situ and ex vivo studies indicate that IL-15 stimulates the accumulation and cytotoxic activation of CD8+ T IEL in active CD, and that of the malignant innate-like IEL in type II refractory CD (RCDII). Other studies show that IL-15 impairs the immunoregulatory control of effector T cells, notably CD8+. Recently, animal models have been designed to investigate the respective role of CD4+ T cells and IL-15 in CD. We discuss more particularly our results in such a model, which shows that IL-15 produced in excess in the intestine can cooperate with CD4+ T cells specific for a dietary antigen to trigger a celiac-like enteropathy. In this mouse model, CD4+ T cells activated by dietary ovalbumin secreted IL-2 which, along with IL-15, stimulated the expansion of noncognate intestinal cytotoxic CD8+ T cells containing large amounts of granzyme B. In the presence of IL-15, the latter cells did not respond to regulatory T cells, and accumulated in the intestine close to epithelial damage. Conclusion: On the basis of these data, we propose that, in CD, gluten-specific CD4+ T cells synthesize cytokines that synergize with IL-15 to license the expansion and activation of cytotoxic IEL, which drive tissue damage. We suggest that IL-15 is a meaningful therapeutic target, notably in patients with RCDII in which malignant IEL can respond to IL-15 independently of signals provided by CD4+ T cells.
MeSH term(s)	Animals ; CD4-Positive T-Lymphocytes/immunology ; Celiac Disease/immunology ; Cytotoxicity, Immunologic ; HLA-DQ Antigens/immunology ; Humans ; Interleukin-15/metabolism ; Intestinal Mucosa/immunology ; Intestinal Mucosa/pathology
Chemical Substances	HLA-DQ Antigens ; Interleukin-15
Language	English
Publishing date	2015-04-22
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	632798-9
ISSN	1421-9875 ; 0257-2753
ISSN (online)	1421-9875
ISSN	0257-2753
DOI	10.1159/000369521
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Zs.A 1853: Show issues

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Article ; Online: Celiac disease: an immunological jigsaw.

Meresse, Bertrand / Malamut, Georgia / Cerf-Bensussan, Nadine

Immunity

2012 Volume 36, Issue 6, Page(s) 907–919

Abstract: Celiac disease (CD) is a chronic enteropathy induced by dietary gluten in genetically predisposed people. The keystone of CD pathogenesis is an adaptive immune response orchestrated by the interplay between gluten and MHC class II HLA-DQ2 and DQ8 ... ...

Abstract	Celiac disease (CD) is a chronic enteropathy induced by dietary gluten in genetically predisposed people. The keystone of CD pathogenesis is an adaptive immune response orchestrated by the interplay between gluten and MHC class II HLA-DQ2 and DQ8 molecules. Yet, other factors that impair immunoregulatory mechanisms and/or activate the large population of intestinal intraepithelial lymphocytes (IEL) are indispensable for driving tissue damage. Herein, we summarize our current understanding of the mechanisms and consequences of the undesirable immune response initiated by gluten peptides. We show that CD is a model disease to decipher the role of MHC class II molecules in human immunopathology, to analyze the mechanisms that link tolerance to food proteins and autoimmunity, and to investigate how chronic activation of IEL can lead to T cell lymphomagenesis.
MeSH term(s)	Adaptive Immunity ; Age of Onset ; Animals ; Autoantibodies/biosynthesis ; Autoantibodies/immunology ; Autoimmune Diseases/epidemiology ; Autoimmune Diseases/immunology ; Celiac Disease/diagnosis ; Celiac Disease/diet therapy ; Celiac Disease/epidemiology ; Celiac Disease/genetics ; Celiac Disease/immunology ; Celiac Disease/pathology ; Comorbidity ; Disease Models, Animal ; Disease Progression ; Food Hypersensitivity/complications ; Food Hypersensitivity/immunology ; GTP-Binding Proteins ; Genes, MHC Class II ; Genetic Predisposition to Disease ; Glutens/adverse effects ; Glutens/chemistry ; HLA-D Antigens/immunology ; Humans ; Immunoglobulin A/immunology ; Interleukin-15/immunology ; Intestinal Mucosa/immunology ; Intestinal Mucosa/pathology ; Lymphocyte Activation/genetics ; Lymphoma, T-Cell/etiology ; Lymphoma, T-Cell/immunology ; Mice ; Models, Immunological ; T-Lymphocyte Subsets/immunology ; Transglutaminases/analysis ; Transglutaminases/immunology ; Transglutaminases/physiology ; Virus Diseases/complications ; Virus Diseases/immunology
Chemical Substances	Autoantibodies ; HLA-D Antigens ; Immunoglobulin A ; Interleukin-15 ; Glutens (8002-80-0) ; transglutaminase 2 (EC 2.3.2.-) ; Transglutaminases (EC 2.3.2.13) ; GTP-Binding Proteins (EC 3.6.1.-)
Language	English
Publishing date	2012-06-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2012.06.006
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Zs.A 4227: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: The role of animal models in unravelling therapeutic targets in coeliac disease.

Costes, Léa M M / Meresse, Bertrand / Cerf-Bensussan, Nadine / Samsom, Janneke N

Best practice & research. Clinical gastroenterology

2015 Volume 29, Issue 3, Page(s) 437–450

Abstract: Coeliac disease is a complex small intestinal enteropathy that develops consequently to a breach of tolerance to gliadin, a storage protein abundantly found in cereals such as wheat, rye and barley. The understanding of the mechanisms underlying the ... ...

Abstract	Coeliac disease is a complex small intestinal enteropathy that develops consequently to a breach of tolerance to gliadin, a storage protein abundantly found in cereals such as wheat, rye and barley. The understanding of the mechanisms underlying the development of coeliac disease in HLA-DQ2 and HLA-DQ8 genetically susceptible individuals has greatly improved during the last decades but so far did not allow to develop curative therapeutics, leaving a long-life gluten free diet as the only treatment option for the patients. In order to bring new therapeutic targets to light and to test the safety and efficacy of putative drugs, animal models recapitulating features of the disease are needed. Here, we will review the existing animal models and the clinical features of coeliac disease they reflect and discuss their relevance for modelling immune pathways that may lead to potential therapeutic approaches.
MeSH term(s)	Animals ; Celiac Disease/immunology ; Celiac Disease/pathology ; Disease Models, Animal ; Genetic Predisposition to Disease ; Humans ; Immune Tolerance/immunology
Language	English
Publishing date	2015-06
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2048181-0
ISSN	1532-1916 ; 1521-6918
ISSN (online)	1532-1916
ISSN	1521-6918
DOI	10.1016/j.bpg.2015.04.007
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