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Article ; Online: Regulation of lymphocyte trafficking in central nervous system autoimmunity.

Oukka, Mohamed / Bettelli, Estelle

2018 Volume 55, Page(s) 38–43

Abstract: ... ...

Abstract	CD4
MeSH term(s)	Animals ; Autoimmunity/immunology ; CD4-Positive T-Lymphocytes/immunology ; Central Nervous System/immunology ; Humans
Language	English
Publishing date	2018-09-27
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1035767-1
ISSN	1879-0372 ; 0952-7915
ISSN (online)	1879-0372
ISSN	0952-7915
DOI	10.1016/j.coi.2018.09.008
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Zs.MG 13: Show issues

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Article ; Online: A BAFFling Association between Malaria Resistance and the Risk of Multiple Sclerosis.

Korn, Thomas / Oukka, Mohamed

The New England journal of medicine

2017 Volume 376, Issue 17, Page(s) 1680–1681

MeSH term(s)	Humans ; Malaria ; Multiple Sclerosis ; Risk
Language	English
Publishing date	2017-04-25
Publishing country	United States
Document type	Editorial
ZDB-ID	207154-x
ISSN	1533-4406 ; 0028-4793
ISSN (online)	1533-4406
ISSN	0028-4793
DOI	10.1056/NEJMe1700720
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Article ; Online: Cutting Edge: DOCK8 Regulates a Subset of Dendritic Cells That Is Critical for the Development of Experimental Autoimmune Encephalomyelitis.

Weliwitigoda, Asanga / Palle, Pushpalatha / Gessner, Melissa / Hubbard, Nicholas W / Oukka, Mohamed / Bettelli, Estelle

Journal of immunology (Baltimore, Md. : 1950)

2021 Volume 207, Issue 10, Page(s) 2417–2422

Abstract: Dedicator of cytokinesis 8 (DOCK8) is a guanine nucleotide exchange factor with an essential role in cytoskeletal rearrangement, cell migration, and survival of various immune cells. Interestingly, DOCK8-deficient mice are resistant to the development of ...

Abstract	Dedicator of cytokinesis 8 (DOCK8) is a guanine nucleotide exchange factor with an essential role in cytoskeletal rearrangement, cell migration, and survival of various immune cells. Interestingly, DOCK8-deficient mice are resistant to the development of experimental autoimmune encephalomyelitis (EAE). To understand if EAE resistance in these mice results from an alteration in dendritic cell (DC) functions, we generated mice with conditional deletion of DOCK8 in DCs and observed attenuated EAE in these mice compared with control mice. Additionally, we demonstrated that DOCK8 is important for the existence of splenic conventional DC2 and lymph node migratory DCs and further established that migratory DC, rather than resident DC, are essential for the generation and proliferation of pathogenic T cell populations upon immunization with myelin Ag in adjuvant. Therefore, our data suggest that limiting migratory DCs through DOCK8 deletion and possibly other mechanisms could limit the development of CNS autoimmunity.
MeSH term(s)	Animals ; Dendritic Cells/immunology ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Female ; Guanine Nucleotide Exchange Factors/immunology ; Male ; Mice ; Mice, Inbred C57BL
Chemical Substances	Dock8 protein, mouse ; Guanine Nucleotide Exchange Factors
Language	English
Publishing date	2021-10-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.2001294
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Article ; Online: Cutting Edge: Systemic Autoimmunity in Murine STAT3 Gain-of-Function Syndrome Is Characterized by Effector T Cell Expansion in the Absence of Overt Regulatory T Cell Dysfunction.

Woods, Jonathan / Pemberton, Sarah E / Largent, Andrea D / Chiang, Kristy / Liggitt, Denny / Oukka, Mohamed / Rawlings, David J / Jackson, Shaun W

Journal of immunology (Baltimore, Md. : 1950)

2022 Volume 209, Issue 6, Page(s) 1033–1038

Abstract: Germline gain-of-function mutations in the transcriptional ... ...

Abstract	Germline gain-of-function mutations in the transcriptional factor
MeSH term(s)	Animals ; Autoimmunity ; CD8-Positive T-Lymphocytes/metabolism ; Cell Differentiation ; Gain of Function Mutation ; Gene Knock-In Techniques ; Humans ; Inflammation/pathology ; Mice ; Mice, Transgenic ; STAT3 Transcription Factor/genetics ; T-Lymphocytes, Regulatory ; Th17 Cells
Chemical Substances	STAT3 Transcription Factor ; STAT3 protein, human ; Stat3 protein, mouse
Language	English
Publishing date	2022-08-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.2100920
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Ud II Zs.37: 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)
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Article ; Online: Angiotensin II-induced a steeper blood pressure elevation in IL-23 receptor-deficient mice: Role of interferon-γ-producing T cells.

Shokoples, Brandon G / Comeau, Kevin / Higaki, Akinori / Ferreira, Nathanne S / Caillon, Antoine / Berillo, Olga / Oukka, Mohamed / Paradis, Pierre / Schiffrin, Ernesto L

Hypertension research : official journal of the Japanese Society of Hypertension

2022 Volume 46, Issue 1, Page(s) 40–49

Abstract: A subset of interleukin (IL)-17A-producing γδ T cells called γδT17 cells may contribute to progression of hypertension. γδT17 cell development is in part dependent upon IL-23 receptor (IL-23R) stimulation. We hypothesized that angiotensin (Ang) II- ... ...

Abstract	A subset of interleukin (IL)-17A-producing γδ T cells called γδT17 cells may contribute to progression of hypertension. γδT17 cell development is in part dependent upon IL-23 receptor (IL-23R) stimulation. We hypothesized that angiotensin (Ang) II-induced blood pressure (BP) elevation and vascular injury would be blunted in Il23r knock-in (Il23r
MeSH term(s)	Animals ; Mice ; Angiotensin II/pharmacology ; Blood Pressure ; CD8-Positive T-Lymphocytes ; Hypertension/chemically induced ; Interferon-gamma ; Mice, Inbred C57BL ; Mice, Knockout ; Receptors, Interleukin/deficiency ; Receptors, Interleukin/genetics
Chemical Substances	Angiotensin II (11128-99-7) ; Interferon-gamma (82115-62-6) ; interleukin-23 receptor, mouse ; Receptors, Interleukin
Language	English
Publishing date	2022-10-15
Publishing country	England
Document type	Journal Article
ZDB-ID	1175297-x
ISSN	1348-4214 ; 0916-9636
ISSN (online)	1348-4214
ISSN	0916-9636
DOI	10.1038/s41440-022-01055-3
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Article: Interplay between pathogenic Th17 and regulatory T cells.

Oukka, Mohamed

Annals of the rheumatic diseases

2007 Volume 66 Suppl 3, Page(s) iii87–90

Abstract: Autoimmune diseases arise from a break in tolerance toward self-antigens and are characterised by the development of pathogenic T cell populations infiltrating the target organ. Regulatory T cells play an important role in maintaining self-tolerance ... ...

Abstract	Autoimmune diseases arise from a break in tolerance toward self-antigens and are characterised by the development of pathogenic T cell populations infiltrating the target organ. Regulatory T cells play an important role in maintaining self-tolerance through their inhibitory functions on effector T cells. The usage of ex vivo-generated regulatory T cells (Treg) has been regarded as a potentially attractive therapeutic approach for autoimmune diseases. However, the dynamics of Treg in autoimmunity are not well understood. Here, we summarise our published findings on the interplay between Treg and Th17 effector cells in vivo during experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis. We have developed Foxp3gfp "knock-in" mice and myelin oligodendrocyte glycoprotein (MOG)(35-55)/IA(b) (MHC class II)-tetramers to track autoantigen-specific Treg in vivo during EAE. On immunisation with MOG, Treg cells were detected in the central nervous system (CNS) as early as day 10. However, at the onset of disease, the accumulation of MOG-specific effector T cells (T-eff) largely prevailed. Subsequently, during remission T-eff rapidly contracted whereas a highly suppressive Treg population persisted in the CNS. The interplay between effector Th17 and Treg extend beyond their functions in vivo as we and others have identified the factors responsible for Th17 differentiation. While TGF-beta is a critical differentiation factor for Treg cells, IL6 completely inhibits the generation of Treg cells induced by TGF-beta. Instead, IL6 and TGF-beta together induce the differentiation of pathogenic Th17 cells. Our data demonstrate a dichotomy in the generation of Th17 cells that induce autoimmunity and Treg cells that inhibit autoimmune tissue injury.
MeSH term(s)	Animals ; Autoantigens/immunology ; Autoimmunity/immunology ; Cell Differentiation/immunology ; Central Nervous System/immunology ; Epitopes/immunology ; Immune Tolerance/immunology ; Immunization/methods ; Mice ; Models, Immunological ; Myelin Proteins ; Myelin Sheath/immunology ; Myelin-Associated Glycoprotein/immunology ; Myelin-Oligodendrocyte Glycoprotein ; T-Lymphocytes, Helper-Inducer/immunology ; T-Lymphocytes, Regulatory/immunology
Chemical Substances	Autoantigens ; Epitopes ; Mog protein, mouse ; Myelin Proteins ; Myelin-Associated Glycoprotein ; Myelin-Oligodendrocyte Glycoprotein
Language	English
Publishing date	2007-10-12
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	7090-7
ISSN	1468-2060 ; 0003-4967
ISSN (online)	1468-2060
ISSN	0003-4967
DOI	10.1136/ard.2007.078527
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Uh III Zs.114: 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 167: Show issues

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Article ; Online: IL-23 stabilizes an effector T

Wertheimer, Tobias / Zwicky, Pascale / Rindlisbacher, Lukas / Sparano, Colin / Vermeer, Marijne / de Melo, Bruno Marcel Silva / Haftmann, Claudia / Rückert, Tamina / Sethi, Aakriti / Schärli, Stefanie / Huber, Anna / Ingelfinger, Florian / Xu, Caroline / Kim, Daehong / Häne, Philipp / Fonseca da Silva, André / Muschaweckh, Andreas / Nunez, Nicolas / Krishnarajah, Sinduya /

Köhler, Natalie / Zeiser, Robert / Oukka, Mohamed / Korn, Thomas / Tugues, Sonia / Becher, Burkhard

Nature immunology

2024 Volume 25, Issue 3, Page(s) 512–524

Abstract: Interleukin-23 (IL-23) is a proinflammatory cytokine mainly produced by myeloid cells that promotes tumor growth in various preclinical cancer models and correlates with adverse outcomes. However, as to how IL-23 fuels tumor growth is unclear. Here, we ... ...

Abstract	Interleukin-23 (IL-23) is a proinflammatory cytokine mainly produced by myeloid cells that promotes tumor growth in various preclinical cancer models and correlates with adverse outcomes. However, as to how IL-23 fuels tumor growth is unclear. Here, we found tumor-associated macrophages to be the main source of IL-23 in mouse and human tumor microenvironments. Among IL-23-sensing cells, we identified a subset of tumor-infiltrating regulatory T (T
MeSH term(s)	Animals ; Humans ; Mice ; Cytokines ; Interleukin-23/genetics ; Neoplasms/genetics ; T-Lymphocytes ; Tumor Microenvironment
Chemical Substances	Cytokines ; Interleukin-23
Language	English
Publishing date	2024-02-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/s41590-024-01755-7
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Zs.A 5294: 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: Interleukin 23 in Crohn's disease.

Eken, Ahmet / Singh, Akhilesh K / Oukka, Mohamed

Inflammatory bowel diseases

2014 Volume 20, Issue 3, Page(s) 587–595

Abstract: Crohn's disease (CD) is a lifelong inflammatory condition with underlying environmental and genetic components. CD affects multiple parts of the gastrointestinal tract, and it has a growing incidence in Western societies. IL-23 receptor variants have ... ...

Abstract	: Crohn's disease (CD) is a lifelong inflammatory condition with underlying environmental and genetic components. CD affects multiple parts of the gastrointestinal tract, and it has a growing incidence in Western societies. IL-23 receptor variants have been identified as susceptibility or resistance factors for CD in genome-wide association studies. Accordingly, IL-23 is required for the development of experimental inflammatory bowel disease in many murine models. IL-23 receptor is expressed by both innate and adaptive immune cells, which include Th17, natural killer T, γδ T cells, and RORγt innate lymphoid cells all of which are capable of secreting IL-17A, IL-17F, IL-22, and interferon-γ upon IL-23 stimulation. During the past decade, pathogenic and protective roles have been described for these cytokines in the inflammatory bowel disease pathogenesis. More recently, innate lymphoid cells have been implicated in disease development. In this review, we have summarized and discussed these findings with an emphasis not only on the contribution of Th17 but also on innate lymphoid cells to disease etiology.
MeSH term(s)	Animals ; Crohn Disease/immunology ; Crohn Disease/metabolism ; Crohn Disease/pathology ; Humans ; Interleukin-23/metabolism
Chemical Substances	Interleukin-23
Language	English
Publishing date	2014-01-29
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1340971-2
ISSN	1536-4844 ; 1078-0998
ISSN (online)	1536-4844
ISSN	1078-0998
DOI	10.1097/01.MIB.0000442014.52661.20
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Article ; Online: IL-23 receptor deficiency results in lower bone mass via indirect regulation of bone formation.

Razawy, Wida / Alves, Celso H / Koedam, Marijke / Asmawidjaja, Patrick S / Mus, Adriana M C / Oukka, Mohamed / Leenen, Pieter J M / Visser, Jenny A / van der Eerden, Bram C J / Lubberts, Erik

Scientific reports

2021 Volume 11, Issue 1, Page(s) 10244

Abstract: The IL-23 receptor (IL-23R) signaling pathway has pleiotropic effects on the differentiation of osteoclasts and osteoblasts, since it can inhibit or stimulate these processes via different pathways. However, the potential role of this pathway in the ... ...

Abstract	The IL-23 receptor (IL-23R) signaling pathway has pleiotropic effects on the differentiation of osteoclasts and osteoblasts, since it can inhibit or stimulate these processes via different pathways. However, the potential role of this pathway in the regulation of bone homeostasis remains elusive. Therefore, we studied the role of IL-23R signaling in physiological bone remodeling using IL-23R deficient mice. Using µCT, we demonstrate that 7-week-old IL-23R
MeSH term(s)	Animals ; Bone Density ; Bone Development ; Bone Remodeling ; Bone and Bones/metabolism ; Bone and Bones/physiology ; Cell Differentiation ; Cells, Cultured ; Female ; Femur/metabolism ; Gene Knock-In Techniques/methods ; Interleukin-23/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Osteoblasts/metabolism ; Osteoclasts/metabolism ; Osteogenesis/genetics ; Osteogenesis/physiology ; Receptors, Interleukin/deficiency ; Receptors, Interleukin/genetics ; Receptors, Interleukin/metabolism
Chemical Substances	Interleukin-23 ; Receptors, Interleukin ; interleukin-23 receptor, mouse
Language	English
Publishing date	2021-05-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-89625-2
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Article ; Online: CD4

Razawy, Wida / Asmawidjaja, Patrick S / Mus, Anne-Marie / Salioska, Nazike / Davelaar, Nadine / Kops, Nicole / Oukka, Mohamed / Alves, C Henrique / Lubberts, Erik

European journal of immunology

2019 Volume 50, Issue 2, Page(s) 245–255

Abstract: IL-23 plays an important role in the development of arthritis and the IL-23 receptor (IL-23R) is expressed on different types of T cells. However, it is not fully clear which IL- ... ...

Abstract	IL-23 plays an important role in the development of arthritis and the IL-23 receptor (IL-23R) is expressed on different types of T cells. However, it is not fully clear which IL-23R
MeSH term(s)	Adoptive Transfer/methods ; Animals ; Arthritis/immunology ; CD4-Positive T-Lymphocytes/immunology ; Disease Models, Animal ; Female ; Inflammation/immunology ; Interleukin-17/immunology ; Interleukin-23/immunology ; Lymphoid Tissue/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Receptors, Antigen, T-Cell, gamma-delta/immunology ; Receptors, CCR6/immunology ; Receptors, Interleukin/immunology ; Th17 Cells/immunology
Chemical Substances	CCR6 protein, mouse ; Interleukin-17 ; Interleukin-23 ; Receptors, Antigen, T-Cell, gamma-delta ; Receptors, CCR6 ; Receptors, Interleukin ; interleukin-23 receptor, mouse
Language	English
Publishing date	2019-11-28
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.201948112
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