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Article ; Online: Dispensable roles of Gsdmd and Ripk3 in sustaining IL-1β production and chronic inflammation in Th17-mediated autoimmune arthritis.

Takeuchi, Yusuke / Ohara, Daiya / Watanabe, Hitomi / Sakaguchi, Noriko / Sakaguchi, Shimon / Kondoh, Gen / Morinobu, Akio / Mimori, Tsuneyo / Hirota, Keiji

Scientific reports

2021 Volume 11, Issue 1, Page(s) 18679

Abstract: Programmed necrosis, such as necroptosis and pyroptosis, is a highly pro-inflammatory cellular event that is associated with chronic inflammation. Although there are various triggers of pyroptosis and necroptosis in autoimmune tissue inflammation and ... ...

Abstract	Programmed necrosis, such as necroptosis and pyroptosis, is a highly pro-inflammatory cellular event that is associated with chronic inflammation. Although there are various triggers of pyroptosis and necroptosis in autoimmune tissue inflammation and subsequent lytic forms of cell death release abundant inflammatory mediators, including damage-associated molecular patterns and IL-1β, capable of amplifying autoimmune Th17 effector functions, it remains largely unclear whether the programs play a crucial role in the pathogenesis of autoimmune arthritis. We herein report that Gasdermin D (Gsdmd) and receptor interacting serine/threonine kinase 3 (Ripk3)-key molecules of pyroptosis and necroptosis, respectively-are upregulated in inflamed synovial tissues, but dispensable for IL-1β production and the development of IL-17-producing T helper (Th17) cell-mediated autoimmune arthritis in SKG mice. Gsdmd
MeSH term(s)	Animals ; Arthritis/immunology ; Autoimmune Diseases/immunology ; Chronic Disease ; Inflammation/immunology ; Intracellular Signaling Peptides and Proteins/physiology ; Mice ; Phosphate-Binding Proteins/physiology ; Receptor-Interacting Protein Serine-Threonine Kinases/physiology ; Th17 Cells/immunology
Chemical Substances	Gsdmd protein, mouse ; Intracellular Signaling Peptides and Proteins ; Phosphate-Binding Proteins ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Ripk3 protein, mouse (EC 2.7.11.1)
Language	English
Publishing date	2021-09-21
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/s41598-021-98145-y
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Macrophage activation syndrome in adult dermatomyositis: a case-based review.

Kishida, Dai / Sakaguchi, Noriko / Ueno, Ken-Ichi / Ushiyama, Satoru / Ichikawa, Takanori / Yoshinaga, Tsuneaki / Shimojima, Yasuhiro / Sekijima, Yoshiki

Rheumatology international

2020 Volume 40, Issue 7, Page(s) 1151–1162

Abstract: Macrophage activation syndrome (MAS) is a severe and life-threatening syndrome associated with autoimmune diseases, characterized by fever, hepatosplenomegaly, and pancytopenia. Dermatomyositis (DM) is one of the causes of MAS; however, its clinical ... ...

Abstract	Macrophage activation syndrome (MAS) is a severe and life-threatening syndrome associated with autoimmune diseases, characterized by fever, hepatosplenomegaly, and pancytopenia. Dermatomyositis (DM) is one of the causes of MAS; however, its clinical characteristics in DM patients remain unclear. This study aimed to present a case of anti-melanoma differentiation-associated gene 5 (MDA5) antibody-positive DM complicated by MAS in a 29-year-old woman and to review the literatures including similar cases. Even though symptoms and cytopenia of our patient were refractory to combination therapy, including glucocorticoids, immunosuppressants, and plasma exchange, the administration of rituximab (RTX) resulted in rapid clinical improvement and glucocorticoid reduction. The literature review revealed 18 adult patients with DM associated MAS. Most patients developed MAS within 3 months from DM onset. A monotherapy of glucocorticoid was insufficient to control the disease, and the mortality of MAS in DM was higher than that of MAS in other rheumatic diseases, despite being treated by various means. RTX may be an effective treatment for patients with DM complicated by MAS who are refractory to conventional therapy. Anti-MDA5 antibody could influence the development of MAS; however, further investigations are needed to elucidate the association between myositis-specific antibody and MAS.
MeSH term(s)	Adult ; Autoantibodies/immunology ; Dermatomyositis/complications ; Dermatomyositis/drug therapy ; Dermatomyositis/immunology ; Dermatomyositis/physiopathology ; Female ; Glucocorticoids/therapeutic use ; Humans ; Immunologic Factors/therapeutic use ; Immunosuppressive Agents/therapeutic use ; Interferon-Induced Helicase, IFIH1/immunology ; Lung Diseases, Interstitial/complications ; Lung Diseases, Interstitial/diagnostic imaging ; Lung Diseases, Interstitial/drug therapy ; Lung Diseases, Interstitial/physiopathology ; Macrophage Activation Syndrome/drug therapy ; Macrophage Activation Syndrome/etiology ; Macrophage Activation Syndrome/immunology ; Plasma Exchange ; Rituximab/therapeutic use ; Tomography, X-Ray Computed
Chemical Substances	Autoantibodies ; Glucocorticoids ; Immunologic Factors ; Immunosuppressive Agents ; Rituximab (4F4X42SYQ6) ; IFIH1 protein, human (EC 3.6.1.-) ; Interferon-Induced Helicase, IFIH1 (EC 3.6.4.13)
Language	English
Publishing date	2020-04-30
Publishing country	Germany
Document type	Case Reports ; Journal Article ; Review
ZDB-ID	8286-7
ISSN	1437-160X ; 0172-8172
ISSN (online)	1437-160X
ISSN	0172-8172
DOI	10.1007/s00296-020-04590-9
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Article ; Online: Normal Pressure Hydrocephalus in Systemic Lupus Erythematosus: A Severe Case of Recurrent Cerebral Infarctions After Ventriculoperitoneal Shunt.

Sakaguchi, Noriko / Shimojima, Yasuhiro / Ushiyama, Satoru / Ichikawa, Takanori / Ikeda, Junji / Ueno, Ken-Ichi / Kishida, Dai / Sekijima, Yoshiki

Journal of clinical rheumatology : practical reports on rheumatic & musculoskeletal diseases

2019 Volume 26, Issue 7, Page(s) e246–e248

MeSH term(s)	Cerebral Infarction/diagnosis ; Cerebral Infarction/etiology ; Humans ; Hydrocephalus, Normal Pressure/diagnosis ; Hydrocephalus, Normal Pressure/surgery ; Lupus Erythematosus, Systemic/complications ; Lupus Erythematosus, Systemic/diagnosis ; Treatment Outcome ; Ventriculoperitoneal Shunt/adverse effects
Language	English
Publishing date	2019-07-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	1283266-2
ISSN	1536-7355 ; 1076-1608
ISSN (online)	1536-7355
ISSN	1076-1608
DOI	10.1097/RHU.0000000000001101
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Zs.A 4815: Show issues

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Article ; Online: Construction of a T cell receptor signaling range for spontaneous development of autoimmune disease.

The Journal of experimental medicine

2022 Volume 220, Issue 2

Abstract: Thymic selection and peripheral activation of conventional T (Tconv) and regulatory T (Treg) cells depend on TCR signaling, whose anomalies are causative of autoimmunity. Here, we expressed in normal mice mutated ZAP-70 molecules with different ... ...

Abstract	Thymic selection and peripheral activation of conventional T (Tconv) and regulatory T (Treg) cells depend on TCR signaling, whose anomalies are causative of autoimmunity. Here, we expressed in normal mice mutated ZAP-70 molecules with different affinities for the CD3 chains, or wild type ZAP-70 at graded expression levels under tetracycline-inducible control. Both manipulations reduced TCR signaling intensity to various extents and thereby rendered those normally deleted self-reactive thymocytes to become positively selected and form a highly autoimmune TCR repertoire. The signal reduction more profoundly affected Treg development and function because their TCR signaling was further attenuated by Foxp3 that physiologically repressed the expression of TCR-proximal signaling molecules, including ZAP-70, upon TCR stimulation. Consequently, the TCR signaling intensity reduced to a critical range generated pathogenic autoimmune Tconv cells and concurrently impaired Treg development/function, leading to spontaneous occurrence of autoimmune/inflammatory diseases, such as autoimmune arthritis and inflammatory bowel disease. These results provide a general model of how altered TCR signaling evokes autoimmune disease.
MeSH term(s)	Animals ; Mice ; Autoimmune Diseases ; Autoimmunity ; Signal Transduction ; T-Lymphocytes, Regulatory ; Receptors, Antigen, T-Cell
Chemical Substances	Receptors, Antigen, T-Cell
Language	English
Publishing date	2022-12-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20220386
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Ua VI Zs.107: 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: Regulatory T cells in immunologic self-tolerance and autoimmune disease.

Sakaguchi, Shimon / Sakaguchi, Noriko

International reviews of immunology

2005 Volume 24, Issue 3-4, Page(s) 211–226

Abstract: Naturally arising CD25+ CD4+ regulatory T cells play key roles in the maintenance of immunologic self-tolerance and negative control of various immune responses. The majority, if not all, of them are produced by the normal thymus as a functionally ... ...

Abstract	Naturally arising CD25+ CD4+ regulatory T cells play key roles in the maintenance of immunologic self-tolerance and negative control of various immune responses. The majority, if not all, of them are produced by the normal thymus as a functionally distinct T-cell subpopulation, and their generation is in part developmentally controlled. Genetic abnormality in the development and function of this population can indeed be a cause of autoimmune disease, immunopathology, and allergy in humans. This regulatory population can be exploited to prevent and treat autoimmune disease by strengthening and reestablishing immunologic self-tolerance.
MeSH term(s)	Antigens, CD/immunology ; Autoimmune Diseases/genetics ; Autoimmune Diseases/immunology ; Humans ; Immune Tolerance ; T-Lymphocytes/immunology
Chemical Substances	Antigens, CD
Language	English
Publishing date	2005-05
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	632825-8
ISSN	1545-5858 ; 0883-0185
ISSN (online)	1545-5858
ISSN	0883-0185
DOI	10.1080/08830180590934976
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Zs.A 2156: Show issues

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Article: Animal models of arthritis caused by systemic alteration of the immune system.

Sakaguchi, Shimon / Sakaguchi, Noriko

Current opinion in immunology

2005 Volume 17, Issue 6, Page(s) 589–594

Abstract: Animal models are instrumental in understanding the etiology and pathogenetic mechanisms of rheumatoid arthritis. Several new mouse models have either been produced, including transgenics, gene-knockouts, and gene knock-ins, or established as a ... ...

Abstract	Animal models are instrumental in understanding the etiology and pathogenetic mechanisms of rheumatoid arthritis. Several new mouse models have either been produced, including transgenics, gene-knockouts, and gene knock-ins, or established as a spontaneous disease due to natural gene mutations. These models are suitable for addressing the roles of T cells, autoantibodies, cytokines and innate immunity in the development and progression of rheumatoid arthritis. In particular, they now provide insights into how systemic alterations of the immune system result in a local development of chronic arthritis that leads to joint destruction.
MeSH term(s)	Animals ; Arthritis, Experimental/immunology ; Arthritis, Experimental/pathology ; Arthritis, Rheumatoid/immunology ; Arthritis, Rheumatoid/pathology ; Autoantibodies/immunology ; Cytokines/physiology ; Disease Models, Animal ; Immunity, Innate ; Mice ; T-Lymphocytes/immunology
Chemical Substances	Autoantibodies ; Cytokines
Language	English
Publishing date	2005-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1035767-1
ISSN	1879-0372 ; 0952-7915
ISSN (online)	1879-0372
ISSN	0952-7915
DOI	10.1016/j.coi.2005.09.017
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Zs.A 2773: 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)
Zs.MG 13: Show issues

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Article ; Online: Strain-Specific Manifestation of Lupus-like Systemic Autoimmunity Caused by

Matsuo, Takashi / Hashimoto, Motomu / Sakaguchi, Shimon / Sakaguchi, Noriko / Ito, Yoshinaga / Hikida, Masaki / Tsuruyama, Tatsuaki / Sakai, Kaoru / Yokoi, Hideki / Shirakashi, Mirei / Tanaka, Masao / Ito, Hiromu / Yoshifuji, Hajime / Ohmura, Koichiro / Fujii, Takao / Mimori, Tsuneyo

Journal of immunology (Baltimore, Md. : 1950)

2019 Volume 202, Issue 11, Page(s) 3161–3172

Abstract: A defect in TCR-proximal signaling is a major characteristic of CD4 T cells in systemic lupus erythematosus; however, it is not fully known how defects in TCR signaling lead to lupus-like systemic autoimmunity characterized by germinal center development ...

Abstract	A defect in TCR-proximal signaling is a major characteristic of CD4 T cells in systemic lupus erythematosus; however, it is not fully known how defects in TCR signaling lead to lupus-like systemic autoimmunity characterized by germinal center development and autoantibody production against nuclear Ags. In this study, we show that SKG mice, which develop autoimmune arthritis in a BALB/c background due to defective TCR signaling by a
MeSH term(s)	Animals ; Antibodies, Antinuclear/metabolism ; Autoimmunity ; CD4-Positive T-Lymphocytes/immunology ; Cell Differentiation ; Cells, Cultured ; Cytokines/metabolism ; Germinal Center/immunology ; Humans ; Lupus Erythematosus, Systemic/genetics ; Lupus Erythematosus, Systemic/immunology ; Lymphocyte Activation ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; Mutation/genetics ; Receptors, Antigen, T-Cell/metabolism ; ZAP-70 Protein-Tyrosine Kinase/genetics
Chemical Substances	Antibodies, Antinuclear ; Cytokines ; Receptors, Antigen, T-Cell ; ZAP-70 Protein-Tyrosine Kinase (EC 2.7.10.2) ; Zap70 protein, mouse (EC 2.7.10.2)
Language	English
Publishing date	2019-04-24
Publishing country	United States
Document type	Journal Article ; 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.1801159
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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)
Zs.MG 28: Show issues

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Article ; Online: Pillars article: immunologic self-tolerance maintained by activated T cells expressing IL-2 receptor α-chains (CD25). Breakdown of a single mechanism of self-tolerance causes various autoimmune diseases. J. Immunol. 1995.

Sakaguchi, Shimon / Sakaguchi, Noriko / Asano, Masanao / Itoh, Misako / Toda, Masaaki

Journal of immunology (Baltimore, Md. : 1950)

2011 Volume 186, Issue 7, Page(s) 3808–3821

MeSH term(s)	Animals ; Autoimmune Diseases/history ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/pathology ; Cells, Cultured ; Disease Models, Animal ; Female ; History, 20th Century ; History, 21st Century ; Humans ; Interleukin-2 Receptor alpha Subunit/history ; Lymphocyte Activation/immunology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Self Tolerance/immunology
Chemical Substances	Interleukin-2 Receptor alpha Subunit
Language	English
Publishing date	2011-04-01
Publishing country	United States
Document type	Biography ; Classical Article ; Historical Article ; 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
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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: Autoimmune Th17 Cells Induced Synovial Stromal and Innate Lymphoid Cell Secretion of the Cytokine GM-CSF to Initiate and Augment Autoimmune Arthritis.

Hirota, Keiji / Hashimoto, Motomu / Ito, Yoshinaga / Matsuura, Mayumi / Ito, Hiromu / Tanaka, Masao / Watanabe, Hitomi / Kondoh, Gen / Tanaka, Atsushi / Yasuda, Keiko / Kopf, Manfred / Potocnik, Alexandre J / Stockinger, Brigitta / Sakaguchi, Noriko / Sakaguchi, Shimon

Immunity

2018 Volume 48, Issue 6, Page(s) 1220–1232.e5

Abstract: Despite the importance of Th17 cells in autoimmune diseases, it remains unclear how they control other inflammatory cells in autoimmune tissue damage. Using a model of spontaneous autoimmune arthritis, we showed that arthritogenic Th17 cells stimulated ... ...

Abstract	Despite the importance of Th17 cells in autoimmune diseases, it remains unclear how they control other inflammatory cells in autoimmune tissue damage. Using a model of spontaneous autoimmune arthritis, we showed that arthritogenic Th17 cells stimulated fibroblast-like synoviocytes via interleukin-17 (IL-17) to secrete the cytokine GM-CSF and also expanded synovial-resident innate lymphoid cells (ILCs) in inflamed joints. Activated synovial ILCs, which expressed CD25, IL-33Ra, and TLR9, produced abundant GM-CSF upon stimulation by IL-2, IL-33, or CpG DNA. Loss of GM-CSF production by either ILCs or radio-resistant stromal cells prevented Th17 cell-mediated arthritis. GM-CSF production by Th17 cells augmented chronic inflammation but was dispensable for the initiation of arthritis. We showed that GM-CSF-producing ILCs were present in inflamed joints of rheumatoid arthritis patients. Thus, a cellular cascade of autoimmune Th17 cells, ILCs, and stromal cells, via IL-17 and GM-CSF, mediates chronic joint inflammation and can be a target for therapeutic intervention.
MeSH term(s)	Animals ; Arthritis, Rheumatoid/immunology ; Arthritis, Rheumatoid/metabolism ; Autoimmune Diseases/immunology ; Autoimmune Diseases/metabolism ; Granulocyte-Macrophage Colony-Stimulating Factor/biosynthesis ; Granulocyte-Macrophage Colony-Stimulating Factor/immunology ; Humans ; Lymphocytes/immunology ; Lymphocytes/metabolism ; Mice ; Stromal Cells/immunology ; Stromal Cells/metabolism ; Synovial Membrane/immunology ; Synovial Membrane/metabolism ; Th17 Cells/immunology ; Th17 Cells/metabolism
Chemical Substances	Granulocyte-Macrophage Colony-Stimulating Factor (83869-56-1)
Language	English
Publishing date	2018-05-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2018.04.009
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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)
Zs.MG 69: Show issues

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Article: Thymus, innate immunity and autoimmune arthritis: Interplay of gene and environment

Sakaguchi, Shimon / Tanaka, Satoshi / Tanaka, Atsushi / Ito, Yoshinaga / Maeda, Shinji / Sakaguchi, Noriko / Hashimoto, Motomu

FEBS letters. 2011 Dec. 1, v. 585, no. 23

2011

Abstract: A hypomorphic mutation of the gene encoding zeta-associated protein-70 (ZAP-70), a signaling molecule in T cells, produces autoimmune arthritis in mice under a microbially conventional condition but not in a clean environment. The genetic anomaly alters ... ...

Abstract	A hypomorphic mutation of the gene encoding zeta-associated protein-70 (ZAP-70), a signaling molecule in T cells, produces autoimmune arthritis in mice under a microbially conventional condition but not in a clean environment. The genetic anomaly alters thymic selection of self-reactive T cells as well as natural regulatory T cells and their respective functions. Highly self-reactive polyclonal T cells, including arthritogenic ones, thus produced by the thymus strongly recognize self-antigens presented by antigen-presenting cells, stimulate them to up-regulate co-stimulatory molecules and secrete cytokines that drive naïve self-reactive T cells to differentiate into autoimmune effector Th17 cells. Administration of microbial products and activation of complement can facilitate the differentiation, evoking clinically overt arthritis in a microbially clean environment. Furthermore, mutation-dependent graded attenuation of T cell receptor signaling alters disease phenotypes and the dependency of disease occurrence on the environment. These findings provide a model of how genetic and environmental factors, in association, cause autoimmune diseases such as rheumatoid arthritis.
Keywords	T-lymphocytes ; antigen-presenting cells ; complement ; cytokines ; disease occurrence ; environmental factors ; genes ; innate immunity ; mice ; models ; mutation ; phenotype ; rheumatoid arthritis
Language	English
Dates of publication	2011-1201
Size	p. 3633-3639.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1016/j.febslet.2011.10.026
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