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Article ; Online: Identification of Tensin-3 as a MALT1 substrate that controls B cell adhesion and lymphoma dissemination.

Juilland, Mélanie / Alouche, Nagham / Ubezzi, Ivana / Gonzalez, Montserrat / Rashid, Harun-Or / Scarpellino, Leonardo / Erdmann, Tabea / Grau, Michael / Lenz, Georg / Luther, Sanjiv A / Thome, Margot

Proceedings of the National Academy of Sciences of the United States of America

2023 Volume 120, Issue 52, Page(s) e2301155120

Abstract: The protease MALT1 promotes lymphocyte activation and lymphomagenesis by cleaving a limited set of cellular substrates, most of which control gene expression. Here, we identified the integrin-binding scaffold protein Tensin-3 as a MALT1 substrate in ... ...

Abstract	The protease MALT1 promotes lymphocyte activation and lymphomagenesis by cleaving a limited set of cellular substrates, most of which control gene expression. Here, we identified the integrin-binding scaffold protein Tensin-3 as a MALT1 substrate in activated human B cells. Activated B cells lacking Tensin-3 showed decreased integrin-dependent adhesion but exhibited comparable NF-κB1 and Jun N-terminal kinase transcriptional responses. Cells expressing a noncleavable form of Tensin-3, on the other hand, showed increased adhesion. To test the role of Tensin-3 cleavage in vivo, mice expressing a noncleavable version of Tensin-3 were generated, which showed a partial reduction in the T cell-dependent B cell response. Interestingly, human diffuse large B cell lymphomas and mantle cell lymphomas with constitutive MALT1 activity showed strong constitutive Tensin-3 cleavage and a decrease in uncleaved Tensin-3 levels. Moreover, silencing of Tensin-3 expression in MALT1-driven lymphoma promoted dissemination of xenografted lymphoma cells to the bone marrow and spleen. Thus, MALT1-dependent Tensin-3 cleavage reveals a unique aspect of the function of MALT1, which negatively regulates integrin-dependent B cell adhesion and facilitates metastatic spread of B cell lymphomas.
MeSH term(s)	Mice ; Humans ; Animals ; Adult ; Tensins/genetics ; Caspases/metabolism ; NF-kappa B/metabolism ; Cell Adhesion/genetics ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein/genetics ; Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein/metabolism ; Lymphoma, Large B-Cell, Diffuse/genetics ; Integrins
Chemical Substances	Tensins ; Caspases (EC 3.4.22.-) ; NF-kappa B ; Neoplasm Proteins ; Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein (EC 3.4.22.-) ; Integrins ; MALT1 protein, human (EC 3.4.22.-)
Language	English
Publishing date	2023-12-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2301155120
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Article ; Online: Fine-tuning of MEK signaling is pivotal for limiting B and T cell activation.

Houde, Nicolas / Beuret, Laurent / Bonaud, Amélie / Fortier-Beaulieu, Simon-Pierre / Truchon-Landry, Kim / Aoidi, Rifdat / Pic, Émilie / Alouche, Nagham / Rondeau, Vincent / Schlecht-Louf, Géraldine / Balabanian, Karl / Espéli, Marion / Charron, Jean

Cell reports

2022 Volume 38, Issue 2, Page(s) 110223

Abstract: MEK1 and MEK2, the only known activators of ERK, are attractive therapeutic candidates for both cancer and autoimmune diseases. However, how MEK signaling finely regulates immune cell activation is only partially understood. To address this question, we ... ...

Abstract	MEK1 and MEK2, the only known activators of ERK, are attractive therapeutic candidates for both cancer and autoimmune diseases. However, how MEK signaling finely regulates immune cell activation is only partially understood. To address this question, we specifically delete Mek1 in hematopoietic cells in the Mek2 null background. Characterization of an allelic series of Mek mutants reveals the presence of distinct degrees of spontaneous B cell activation, which are inversely proportional to the levels of MEK proteins and ERK activation. While Mek1 and Mek2 null mutants have a normal lifespan, 1Mek1 and 1Mek2 mutants retaining only one functional Mek1 or Mek2 allele in hematopoietic cell lineages die from glomerulonephritis and lymphoproliferative disorders, respectively. This establishes that the fine-tuning of the ERK/MAPK pathway is critical to regulate B and T cell activation and function and that each MEK isoform plays distinct roles during lymphocyte activation and disease development.
MeSH term(s)	Alleles ; Animals ; B-Lymphocytes/metabolism ; Female ; Humans ; Lymphocyte Activation/genetics ; Lymphocyte Activation/physiology ; MAP Kinase Kinase 1/metabolism ; MAP Kinase Kinase 1/physiology ; MAP Kinase Kinase 2/genetics ; MAP Kinase Kinase 2/metabolism ; MAP Kinase Kinase 2/physiology ; MAP Kinase Signaling System/genetics ; MAP Kinase Signaling System/physiology ; Male ; Mice ; Mice, 129 Strain ; Mitogen-Activated Protein Kinase 1/metabolism ; Phosphorylation ; Signal Transduction/physiology ; T-Lymphocytes/metabolism
Chemical Substances	Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; MAP Kinase Kinase 1 (EC 2.7.12.2) ; MAP Kinase Kinase 2 (EC 2.7.12.2) ; Map2k1 protein, mouse (EC 2.7.12.2) ; Map2k2 protein, mouse (EC 2.7.12.2)
Language	English
Publishing date	2022-01-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2021.110223
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Article ; Online: Sec22b is a critical and nonredundant regulator of plasma cell maintenance.

Bonaud, Amélie / Gargowitsch, Laetitia / Gilbert, Simon M / Rajan, Elanchezhian / Canales-Herrerias, Pablo / Stockholm, Daniel / Rahman, Nabila F / Collins, Mark O / Taskiran, Hakan / Hill, Danika L / Alloatti, Andres / Alouche, Nagham / Balor, Stéphanie / Soldan, Vanessa / Gillet, Daniel / Barbier, Julien / Bachelerie, Françoise / Smith, Kenneth G C / Jellusova, Julia /

Bruhns, Pierre / Amigorena, Sebastian / Balabanian, Karl / Linterman, Michelle A / Peden, Andrew A / Espéli, Marion

Proceedings of the National Academy of Sciences of the United States of America

2023 Volume 120, Issue 2, Page(s) e2213056120

Abstract: Despite the essential role of plasma cells in health and disease, the cellular mechanisms controlling their survival and secretory capacity are still poorly understood. Here, we identified the soluble N-ethylmaleimide-sensitive factor attachment protein ... ...

Abstract	Despite the essential role of plasma cells in health and disease, the cellular mechanisms controlling their survival and secretory capacity are still poorly understood. Here, we identified the soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) Sec22b as a unique and critical regulator of plasma cell maintenance and function. In the absence of Sec22b, plasma cells were hardly detectable and serum antibody titers were dramatically reduced. Accordingly,
MeSH term(s)	Mice ; Animals ; Plasma Cells/metabolism ; R-SNARE Proteins/metabolism ; SNARE Proteins/metabolism ; Endoplasmic Reticulum/metabolism ; Biological Transport
Chemical Substances	R-SNARE Proteins ; SNARE Proteins ; Sec22b protein, mouse
Language	English
Publishing date	2023-01-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2213056120
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Zs.A 1148: Show issues

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Article ; Online: FcγRIIb differentially regulates pre-immune and germinal center B cell tolerance in mouse and human.

Espéli, Marion / Bashford-Rogers, Rachael / Sowerby, John M / Alouche, Nagham / Wong, Limy / Denton, Alice E / Linterman, Michelle A / Smith, Kenneth G C

Nature communications

2019 Volume 10, Issue 1, Page(s) 1970

Abstract: Several tolerance checkpoints exist throughout B cell development to control autoreactive B cells and prevent the generation of pathogenic autoantibodies. FcγRIIb is an Fc receptor that inhibits B cell activation and, if defective, is associated with ... ...

Abstract	Several tolerance checkpoints exist throughout B cell development to control autoreactive B cells and prevent the generation of pathogenic autoantibodies. FcγRIIb is an Fc receptor that inhibits B cell activation and, if defective, is associated with autoimmune disease, yet its impact on specific B cell tolerance checkpoints is unknown. Here we show that reduced expression of FcγRIIb enhances the deletion and anergy of autoreactive immature B cells, but in contrast promotes autoreactive B cell expansion in the germinal center and serum autoantibody production, even in response to exogenous, non-self antigens. Our data thus show that FcγRIIb has opposing effects on pre-immune and post-immune tolerance checkpoints, and suggest that B cell tolerance requires the control of bystander germinal center B cells with low or no affinity for the immunizing antigen.
MeSH term(s)	Algorithms ; Animals ; B-Lymphocytes/immunology ; Cell Differentiation/physiology ; Cell Proliferation/physiology ; Enzyme-Linked Immunosorbent Assay ; Female ; Flow Cytometry ; Germinal Center ; Humans ; Immune Tolerance/immunology ; Leukocytes, Mononuclear/immunology ; Leukocytes, Mononuclear/metabolism ; Male ; Mice ; Receptors, IgG/genetics ; Receptors, IgG/metabolism ; Software
Chemical Substances	Receptors, IgG
Language	English
Publishing date	2019-04-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-019-09434-0
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Article ; Online: CXCR4 Antagonist in HPV5-Associated Perianal Squamous-Cell Carcinoma.

Marin-Esteban, Viviana / Molet, Lucie / Laganà, Marta / Ciocan, Dragos / Dominguez-Lafage, Clément / Alouche, Nagham / Nguyen, Julie / Gallego, Carmen / Mercier-Nomé, Françoise / Jaracz-Ros, Agnieszka / Beaupain, Blandine / Bouligand, Jérôme / Proust, Alexis / Habib, Christophe / Bonnin, Rémy A / Girlich, Delphine / Fouyssac, Fanny / Schmutz, Jean-Luc / Bursztejn, Anne-Claire /

Bellanné-Chantelot, Christine / Bourrat, Emmanuelle / Herfs, Michael / Espéli, Marion / Balabanian, Karl / Schlecht-Louf, Géraldine / Donadieu, Jean / Bachelerie, Françoise / Deback, Claire

The New England journal of medicine

2024 Volume 390, Issue 14, Page(s) 1339–1341

MeSH term(s)	Humans ; Antineoplastic Agents/therapeutic use ; Antiviral Agents/therapeutic use ; Anus Neoplasms/drug therapy ; Anus Neoplasms/virology ; Betapapillomavirus ; Carcinoma, Squamous Cell/drug therapy ; Carcinoma, Squamous Cell/virology ; Receptors, CXCR4/antagonists & inhibitors ; Papillomavirus Infections/complications ; Papillomavirus Infections/drug therapy ; Papillomavirus Infections/virology ; Primary Immunodeficiency Diseases/drug therapy ; Primary Immunodeficiency Diseases/genetics ; Primary Immunodeficiency Diseases/virology ; Warts/drug therapy ; Warts/genetics ; Warts/virology ; Gain of Function Mutation
Chemical Substances	Antineoplastic Agents ; Antiviral Agents ; CXCR4 protein, human ; plerixafor (S915P5499N) ; Receptors, CXCR4
Language	English
Publishing date	2024-04-20
Publishing country	United States
Document type	Letter
ZDB-ID	207154-x
ISSN	1533-4406 ; 0028-4793
ISSN (online)	1533-4406
ISSN	0028-4793
DOI	10.1056/NEJMc2213180
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Article ; Online: Fibroblast-derived IL-33 is dispensable for lymph node homeostasis but critical for CD8 T-cell responses to acute and chronic viral infection.

Aparicio-Domingo, Patricia / Cannelle, Hélène / Buechler, Matthew B / Nguyen, Sylvain / Kallert, Sandra M / Favre, Stéphanie / Alouche, Nagham / Papazian, Natalie / Ludewig, Burkhard / Cupedo, Tom / Pinschewer, Daniel D / Turley, Shannon J / Luther, Sanjiv A

European journal of immunology

2020 Volume 51, Issue 1, Page(s) 76–90

Abstract: Upon viral infection, stressed or damaged cells can release alarmins like IL-33 that act as endogenous danger signals alerting innate and adaptive immune cells. IL-33 coming from nonhematopoietic cells has been identified as important factor triggering ... ...

Abstract	Upon viral infection, stressed or damaged cells can release alarmins like IL-33 that act as endogenous danger signals alerting innate and adaptive immune cells. IL-33 coming from nonhematopoietic cells has been identified as important factor triggering the expansion of antiviral CD8
MeSH term(s)	Acute Disease ; Adaptive Immunity ; Animals ; CD8-Positive T-Lymphocytes/immunology ; Chronic Disease ; Endothelial Cells/immunology ; Fibroblasts/immunology ; Homeostasis ; Humans ; Immunity, Innate ; Interleukin-33/deficiency ; Interleukin-33/genetics ; Interleukin-33/metabolism ; Lymph Nodes/immunology ; Lymphocytic Choriomeningitis/immunology ; Lymphocytic choriomeningitis virus/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Models, Immunological
Chemical Substances	IL33 protein, human ; Il33 protein, mouse ; Interleukin-33
Language	English
Publishing date	2020-08-05
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.201948413
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Zs.A 489: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Hematologic disorder-associated Cxcr4 gain-of-function mutation leads to uncontrolled extrafollicular immune response.

Alouche, Nagham / Bonaud, Amélie / Rondeau, Vincent / Hussein-Agha, Rim / Nguyen, Julie / Bisio, Valeria / Khamyath, Mélanie / Crickx, Etienne / Setterblad, Niclas / Dulphy, Nicolas / Mahevas, Matthieu / McDermott, David H / Murphy, Philip M / Balabanian, Karl / Espéli, Marion

Blood

2021 Volume 137, Issue 22, Page(s) 3050–3063

Abstract: The extrafollicular immune response is essential to generate a rapid but transient wave of protective antibodies during infection. Despite its importance, the molecular mechanisms controlling this first response are poorly understood. Here, we ... ...

Abstract	The extrafollicular immune response is essential to generate a rapid but transient wave of protective antibodies during infection. Despite its importance, the molecular mechanisms controlling this first response are poorly understood. Here, we demonstrate that enhanced Cxcr4 signaling caused by defective receptor desensitization leads to exacerbated extrafollicular B-cell response. Using a mouse model bearing a gain-of-function mutation of Cxcr4 described in 2 human hematologic disorders, warts, hypogammaglobulinemia, infections, and myelokathexis (WHIM) syndrome and Waldenström macroglobulinemia, we demonstrated that mutant B cells exhibited enhanced mechanistic target of rapamycin signaling, cycled more, and differentiated more potently into plasma cells than wild-type B cells after Toll-like receptor (TLR) stimulation. Moreover, Cxcr4 gain of function promoted enhanced homing and persistence of immature plasma cells in the bone marrow, a phenomenon recapitulated in WHIM syndrome patient samples. This translated in increased and more sustained production of antibodies after T-independent immunization in Cxcr4 mutant mice. Thus, our results establish that fine-tuning of Cxcr4 signaling is essential to limit the strength and length of the extrafollicular immune response.
MeSH term(s)	Animals ; Gain of Function Mutation ; Hematologic Diseases/genetics ; Hematologic Diseases/immunology ; Humans ; Mice ; Mice, Transgenic ; Plasma Cells/immunology ; Receptors, CXCR4/genetics ; Receptors, CXCR4/immunology ; Signal Transduction/genetics ; Signal Transduction/immunology ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/immunology
Chemical Substances	CXCR4 protein, mouse ; Receptors, CXCR4 ; mTOR protein, mouse (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2021-02-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2020007450
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Uh III Zs.140: 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.MO 364: Show issues

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Article ; Online: Efficient Plasma Cell Differentiation and Trafficking Require Cxcr4 Desensitization.

Biajoux, Vincent / Natt, Jessica / Freitas, Christelle / Alouche, Nagham / Sacquin, Antoine / Hemon, Patrice / Gaudin, Françoise / Fazilleau, Nicolas / Espéli, Marion / Balabanian, Karl

Cell reports

2016 Volume 17, Issue 1, Page(s) 193–205

Abstract: CXCR4 plays a central role in B cell immune response, notably by promoting plasma cell (PC) migration and maintenance in the bone marrow (BM). Gain-of-function mutations in CXCR4 affecting receptor desensitization have been reported in the rare ... ...

Abstract	CXCR4 plays a central role in B cell immune response, notably by promoting plasma cell (PC) migration and maintenance in the bone marrow (BM). Gain-of-function mutations in CXCR4 affecting receptor desensitization have been reported in the rare immunodeficiency called WHIM syndrome (WS). Despite lymphopenia, patients mount an immune response but fail to maintain it over time. Using a knockin mouse model phenocopying WS, we showed that, counter-intuitively, a gain of Cxcr4 function inhibited the maintenance of antibody titers after immunization. Although the Cxcr4 mutation intrinsically and locally promoted germinal center response and PC differentiation, antigen-specific PCs were barely detected in the BM, a defect mirrored by early accumulation of immature plasmablasts potentially occupying the survival niches for long-lived PCs. Therefore, fine-tuning of Cxcr4 desensitization is critically required for efficient PC differentiation and maintenance, and absence of such a regulatory process may account for the defective humoral immunity observed in WS patients.
MeSH term(s)	Animals ; Antibodies/blood ; B-Lymphocyte Subsets/drug effects ; B-Lymphocyte Subsets/immunology ; B-Lymphocyte Subsets/pathology ; Bone Marrow/drug effects ; Bone Marrow/immunology ; Bone Marrow/pathology ; Cell Differentiation ; Cell Movement ; Desensitization, Immunologic ; Disease Models, Animal ; Gene Expression ; Gene Knock-In Techniques ; Germinal Center ; Haptens ; Hemocyanins/administration & dosage ; Humans ; Immunity, Humoral ; Immunization ; Immunologic Deficiency Syndromes/genetics ; Immunologic Deficiency Syndromes/immunology ; Immunologic Deficiency Syndromes/pathology ; Mice ; Mice, Transgenic ; Ovalbumin/administration & dosage ; Plasma Cells/drug effects ; Plasma Cells/immunology ; Plasma Cells/pathology ; Receptors, CXCR4/genetics ; Receptors, CXCR4/immunology ; Signal Transduction ; Warts/genetics ; Warts/immunology ; Warts/pathology
Chemical Substances	4-hydroxy-3-nitrophenylacetyl-keyhole limpet hemocyanin ; Antibodies ; CXCR4 protein, mouse ; Haptens ; Receptors, CXCR4 ; Ovalbumin (9006-59-1) ; Hemocyanins (9013-72-3)
Language	English
Publishing date	2016-09-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2016.08.068
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Article ; Online: Identification of Tensin-3 as a MALT1 substrate that controls B cell adhesion and lymphoma dissemination.

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Article ; Online: Fine-tuning of MEK signaling is pivotal for limiting B and T cell activation.

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Article ; Online: Sec22b is a critical and nonredundant regulator of plasma cell maintenance.

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Article ; Online: FcγRIIb differentially regulates pre-immune and germinal center B cell tolerance in mouse and human.

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Article ; Online: CXCR4 Antagonist in HPV5-Associated Perianal Squamous-Cell Carcinoma.

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Article ; Online: Fibroblast-derived IL-33 is dispensable for lymph node homeostasis but critical for CD8 T-cell responses to acute and chronic viral infection.

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Article ; Online: Hematologic disorder-associated Cxcr4 gain-of-function mutation leads to uncontrolled extrafollicular immune response.

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Article ; Online: Efficient Plasma Cell Differentiation and Trafficking Require Cxcr4 Desensitization.

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