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Article ; Online: SKI Regulates Medullary Thymic Epithelial Cell Differentiation to Control Peripheral T Cell Responses in Mice.

Chiu, Honyin / Weinstein, Kristin N / Spath, Sabine / Hu, Alex / Varela, Stephanie / Obata-Ninomiya, Kazushige / Ziegler, Steven F

Journal of immunology (Baltimore, Md. : 1950)

2024

Abstract: The thymus is an important site for the establishment of an appropriate immune response through positive and negative selection of developing T cells. During selection, developing T cells interact with cortical and medullary thymic epithelial cells (TECs) ...

Abstract	The thymus is an important site for the establishment of an appropriate immune response through positive and negative selection of developing T cells. During selection, developing T cells interact with cortical and medullary thymic epithelial cells (TECs), termed cTECs and mTECs, respectively. Using a Foxn1Cre+/-SKIfl/fl mouse model, we found that TEC-specific deletion of SKI reduced the mTEC compartment in the thymus and that tissue-restricted Ag expression in mTECs was altered. This decrease in the medullary area led to a decrease in CD4 thymocyte cellularity; however, mature CD4 cellularity in the spleen remained normal. Interestingly, naive CD4 T cells purified from SKI-deleted mice showed a defect in proliferation in vitro after global TCR stimulation, and these mice were significantly protected from developing experimental autoimmune encephalomyelitis compared with the control mice. Overall, our findings suggest that SKI signaling in the thymus regulates mTEC differentiation and function as well as downstream peripheral T cell responses and provide evidence for targeting SKI in T cell-driven autoimmune diseases such as multiple sclerosis.
Language	English
Publishing date	2024-05-20
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.2300262
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Article ; Online: Basophils and Eosinophils in Nematode Infections.

Obata-Ninomiya, Kazushige / Domeier, Phillip P / Ziegler, Steven F

Frontiers in immunology

2020 Volume 11, Page(s) 583824

Abstract: Helminths remain one of the most prolific pathogens in the world. Following infection helminths interact with various epithelial cell surfaces, including skin, lung, and gut. Recent works have shown that epithelial cells produce a series of cytokines ... ...

Abstract	Helminths remain one of the most prolific pathogens in the world. Following infection helminths interact with various epithelial cell surfaces, including skin, lung, and gut. Recent works have shown that epithelial cells produce a series of cytokines such as TSLP, IL-33, and IL-25 that lead to the induction of innate and acquired type 2 immune responses, which we named Type 2 epithelial cytokines. Although basophils and eosinophils are relatively rare granulocytes under normal conditions (0.5% and 5% in peripheral blood, respectively), both are found with increased frequency in type 2 immunity, including allergy and helminth infections. Recent reports showed that basophils and eosinophils not only express effector functions in type 2 immune reactions, but also manipulate the response toward helminths. Furthermore, basophils and eosinophils play non-redundant roles in distinct responses against various nematodes, providing the potential to intervene at different stages of nematode infection. These findings would be helpful to establish vaccination or therapeutic drugs against nematode infections.
MeSH term(s)	Animals ; Basophils/immunology ; Eosinophils/immunology ; Helminths/immunology ; Humans ; Immunity/immunology ; Nematode Infections/immunology
Language	English
Publishing date	2020-11-27
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.583824
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Article ; Online: Emerging role for thymic stromal lymphopoietin-responsive regulatory T cells in colorectal cancer progression in humans and mice.

Obata-Ninomiya, Kazushige / de Jesus Carrion, Steven / Hu, Alex / Ziegler, Steven F

Science translational medicine

2022 Volume 14, Issue 645, Page(s) eabl6960

Abstract: Recruitment of regulatory T cells ( ... ...

Abstract	Recruitment of regulatory T cells (T
MeSH term(s)	Animals ; Colorectal Neoplasms/metabolism ; Cytokines/metabolism ; Humans ; Mice ; Receptors, Cytokine/metabolism ; T-Lymphocytes, Regulatory
Chemical Substances	Cytokines ; Receptors, Cytokine ; thymic stromal lymphopoietin (GT0IL38SP4)
Language	English
Publishing date	2022-05-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.abl6960
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Article ; Online: Epithelial cell-derived cytokines: more than just signaling the alarm.

Roan, Florence / Obata-Ninomiya, Kazushige / Ziegler, Steven F

The Journal of clinical investigation

2019 Volume 129, Issue 4, Page(s) 1441–1451

Abstract: The epithelial cell-derived cytokines thymic stromal lymphopoietin (TSLP), IL-33, and IL-25 are central regulators of type 2 immunity, which drives a broad array of allergic responses. Often characterized as "alarmins" that are released by the barrier ... ...

Abstract	The epithelial cell-derived cytokines thymic stromal lymphopoietin (TSLP), IL-33, and IL-25 are central regulators of type 2 immunity, which drives a broad array of allergic responses. Often characterized as "alarmins" that are released by the barrier epithelium in response to external insults, these epithelial cell-derived cytokines were initially thought to act only early in allergic inflammation. Indeed, TSLP can condition dendritic cells to initiate type 2 responses, and IL-33 may influence susceptibility to asthma through its role in establishing the immune environment in the perinatal lungs. However, TSLP, IL-33, and IL-25 all regulate a broad spectrum of innate immune cell populations and are particularly potent in eliciting and activating type 2 innate lymphoid cells (ILC2s) that may act throughout allergic inflammation. Recent data suggest that a TSLP/ILC axis may mediate steroid resistance in asthma. Recent identification of memory Th2 cell subsets that are characterized by high receptor expression for TSLP, IL-33, and IL-25 further supports a role for these cytokines in allergic exacerbations. There is therefore growing interest in developing biologics that target TSLP, IL-33, and IL-25. This Review provides an overview of TSLP, IL-33, and IL-25 and the development of blocking antibodies that target these epithelial cell-derived cytokines.
MeSH term(s)	Animals ; Cytokines/immunology ; Epithelial Cells/immunology ; Epithelial Cells/pathology ; Humans ; Hypersensitivity/immunology ; Hypersensitivity/pathology ; Immunity, Innate ; Lymphocytes/immunology ; Lymphocytes/pathology
Chemical Substances	Cytokines
Language	English
Publishing date	2019-04-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI124606
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Article ; Online: CBLB

Song, Jing / Anderson, Warren / Hu, Alex / Obata-Ninomiya, Kazushige / Ziegler, Steven F / Rawlings, David J / Buckner, Jane H

Journal of immunology (Baltimore, Md. : 1950)

2022 Volume 209, Issue 7, Page(s) 1260–1271

Abstract: Cbl-b is a negative regulator of T cell activation, and in murine models, a lack ... ...

Abstract	Cbl-b is a negative regulator of T cell activation, and in murine models, a lack of
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Autoimmune Diseases/metabolism ; CD4-Positive T-Lymphocytes ; Cytokines/metabolism ; Humans ; Interleukin-2/genetics ; Interleukin-2/metabolism ; Mice ; Proto-Oncogene Proteins c-cbl/genetics ; Proto-Oncogene Proteins c-cbl/metabolism ; Puromycin ; RNA/metabolism ; T-Lymphocytes, Regulatory
Chemical Substances	Adaptor Proteins, Signal Transducing ; Cytokines ; Interleukin-2 ; Puromycin (4A6ZS6Q2CL) ; RNA (63231-63-0) ; CBLB protein, human (EC 2.3.2.27) ; Proto-Oncogene Proteins c-cbl (EC 2.3.2.27)
Language	English
Publishing date	2022-09-07
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.2200219
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Article ; Online: Regulatory T cells suppress CD4+ effector T cell activation by controlling protein synthesis.

So, Lomon / Obata-Ninomiya, Kazushige / Hu, Alex / Muir, Virginia S / Takamori, Ayako / Song, Jing / Buckner, Jane H / Savan, Ram / Ziegler, Steven F

The Journal of experimental medicine

2023 Volume 220, Issue 3

Abstract: Regulatory T cells (Tregs) suppress the activation and subsequent effector functions of CD4 effector T cells (Teffs). However, molecular mechanisms that enforce Treg-mediated suppression in CD4 Teff are unclear. We found that Tregs suppressed activation- ... ...

Abstract	Regulatory T cells (Tregs) suppress the activation and subsequent effector functions of CD4 effector T cells (Teffs). However, molecular mechanisms that enforce Treg-mediated suppression in CD4 Teff are unclear. We found that Tregs suppressed activation-induced global protein synthesis in CD4 Teffs prior to cell division. We analyzed genome-wide changes in the transcriptome and translatome of activated CD4 Teffs. We show that mRNAs encoding for the protein synthesis machinery are regulated at the level of translation in activated CD4 Teffs by Tregs. Tregs suppressed global protein synthesis of CD4 Teffs by specifically inhibiting mRNAs of the translation machinery at the level of mTORC1-mediated translation control through concerted action of immunosuppressive cytokines IL-10 and TGFβ. Lastly, we found that the therapeutic targeting of protein synthesis with the RNA helicase eIF4A inhibitor rocaglamide A can alleviate inflammatory CD4 Teff activation caused by acute Treg depletion in vivo. These data show that peripheral tolerance is enforced by Tregs through mRNA translational control in CD4 Teffs.
MeSH term(s)	T-Lymphocytes, Regulatory ; CD4-Positive T-Lymphocytes ; Lymphocyte Activation ; Cytokines/metabolism ; Transforming Growth Factor beta/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism
Chemical Substances	Cytokines ; Transforming Growth Factor beta ; RNA, Messenger
Language	English
Publishing date	2023-01-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20221676
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Article ; Online: IL-33/ST2 contributes to severe symptoms in Plasmodium chabaudi-infected BALB/c mice.

Seki, Takenori / Obata-Ninomiya, Kazushige / Shimogawara-Furushima, Rieko / Arai, Toshio / Akao, Nobuaki / Hoshino, Tomoaki / Ohta, Nobuo

Parasitology international

2018 Volume 67, Issue 1, Page(s) 64–69

Abstract: It has been reported that IL-33 contributes to potentiation of Th2 inflammatory diseases and protection against helminth infection. Increased plasma IL-33 levels have been observed in patients with severe falciparum malaria, however, the role of IL-33 in ...

Abstract	It has been reported that IL-33 contributes to potentiation of Th2 inflammatory diseases and protection against helminth infection. Increased plasma IL-33 levels have been observed in patients with severe falciparum malaria, however, the role of IL-33 in malaria remains unclear. Here we report that IL-33 enhances inflammatory responses in malaria infection. ST2-deficiency altered severity of inflammation in the liver and serum levels of pro-inflammatory cytokines such as TNF-α and IL-6, and IL-13 that is a Th2 cytokine during Plasmodium chabaudi infection. IL-13-deficient mice have similar phenotype with ST2-deficient mice during P. chabaudi infection. Furthermore, ST2- and IL-13-deficiency reduced mortality from P. chabaudi infection. These results indicate that IL-33/ST2 can induce production of proinflammatory cytokines, such as TNF-α and IL-6, through production of IL-13 in P. chabaudi-infected BALB/c mice, suggesting that IL-33/ST2 play a critical role in inflammatory responses to malaria infection. Thus, these findings may define a novel therapeutic target for patients with severe malaria.
Language	English
Publishing date	2018-02
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1363151-2
ISSN	1873-0329 ; 1383-5769
ISSN (online)	1873-0329
ISSN	1383-5769
DOI	10.1016/j.parint.2017.03.008
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Article ; Online: ACC1 determines memory potential of individual CD4

Endo, Yusuke / Onodera, Atsushi / Obata-Ninomiya, Kazushige / Koyama-Nasu, Ryo / Asou, Hikari K / Ito, Toshihiro / Yamamoto, Takeshi / Kanno, Toshio / Nakajima, Takahiro / Ishiwata, Kenji / Kanuka, Hirotaka / Tumes, Damon J / Nakayama, Toshinori

Nature metabolism

2019 Volume 1, Issue 2, Page(s) 261–275

Abstract: Immunological memory is central to adaptive immunity and protection from disease. Changing metabolic demands as antigen-specific T cells transition from effector to memory cells have been well documented, but the cell-specific pathways and molecules that ...

Abstract	Immunological memory is central to adaptive immunity and protection from disease. Changing metabolic demands as antigen-specific T cells transition from effector to memory cells have been well documented, but the cell-specific pathways and molecules that govern this transition are poorly defined. Here we show that genetic deletion of ACC1, a rate-limiting enzyme in fatty acid biosynthesis, enhances the formation of CD4
MeSH term(s)	Acetyl-CoA Carboxylase/physiology ; Animals ; CD4-Positive T-Lymphocytes/immunology ; Cell Lineage ; Fatty Acids/biosynthesis ; Immunologic Memory/physiology ; Mice ; Mice, Inbred BALB C
Chemical Substances	Fatty Acids ; ACC1 protein, mouse (EC 6.4.1.2) ; Acetyl-CoA Carboxylase (EC 6.4.1.2)
Language	English
Publishing date	2019-01-14
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2522-5812
ISSN (online)	2522-5812
DOI	10.1038/s42255-018-0025-4
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Article ; Online: CXCR6

Obata-Ninomiya, Kazushige / Ishiwata, Kenji / Nakano, Hisanobu / Endo, Yusuke / Ichikawa, Tomomi / Onodera, Atsushi / Hirahara, Kiyoshi / Okamoto, Yoshitaka / Kanuka, Hirotaka / Nakayama, Toshinori

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

2018 Volume 115, Issue 42, Page(s) E9849–E9858

Abstract: Memory T helper (mTh) cells play important roles in the reinfection of pathogens and drive the pathogenesis of diseases. While recent studies have characterized the pathogenic mTh2 cell subpopulations driving allergic inflammation, those that induce ... ...

Abstract	Memory T helper (mTh) cells play important roles in the reinfection of pathogens and drive the pathogenesis of diseases. While recent studies have characterized the pathogenic mTh2 cell subpopulations driving allergic inflammation, those that induce immune responses against helminth infection remain unknown. We found that IL-5-producing CXCR6
MeSH term(s)	Animals ; Eosinophils/immunology ; Eosinophils/metabolism ; Eosinophils/parasitology ; Fertility/immunology ; Fertility/physiology ; Immunologic Memory/immunology ; Inflammation/immunology ; Inflammation/metabolism ; Inflammation/prevention & control ; Interleukin-1 Receptor-Like 1 Protein/metabolism ; Lung/immunology ; Lung/metabolism ; Lung/parasitology ; Mice ; Mice, Inbred BALB C ; Myelin Basic Protein/metabolism ; Nippostrongylus/immunology ; Receptors, CXCR6/metabolism ; Receptors, Interleukin/metabolism ; Strongylida Infections/complications ; Strongylida Infections/parasitology ; T-Lymphocytes, Regulatory/immunology ; Th1 Cells/immunology ; Th1 Cells/metabolism ; Th2 Cells/immunology ; Th2 Cells/metabolism
Chemical Substances	Cxcr6 protein, mouse ; Il1rl1 protein, mouse ; Interleukin-1 Receptor-Like 1 Protein ; Mbp protein, mouse ; Myelin Basic Protein ; Receptors, CXCR6 ; Receptors, Interleukin
Language	English
Publishing date	2018-10-01
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.1714731115
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Article ; Online: Ezh2 controls development of natural killer T cells, which cause spontaneous asthma-like pathology.

Tumes, Damon / Hirahara, Kiyoshi / Papadopoulos, Magdalene / Shinoda, Kenta / Onodera, Atsushi / Kumagai, Jin / Yip, Kwok Ho / Pant, Harshita / Kokubo, Kota / Kiuchi, Masahiro / Aoki, Ami / Obata-Ninomiya, Kazushige / Tokoyoda, Koji / Endo, Yusuke / Kimura, Motoko Y / Nakayama, Toshinori

The Journal of allergy and clinical immunology

2019 Volume 144, Issue 2, Page(s) 549–560.e10

Abstract: Background: Natural killer T (NKT) cells express a T-cell receptor that recognizes endogenous and environmental glycolipid antigens. Several subsets of NKT cells have been identified, including IFN-γ-producing NKT1 cells, IL-4-producing NKT2 cells, and ... ...

Abstract	Background: Natural killer T (NKT) cells express a T-cell receptor that recognizes endogenous and environmental glycolipid antigens. Several subsets of NKT cells have been identified, including IFN-γ-producing NKT1 cells, IL-4-producing NKT2 cells, and IL-17-producing NKT17 cells. However, little is known about the factors that regulate their differentiation and respective functions within the immune system. Objective: We sought to determine whether the polycomb repressive complex 2 protein enhancer of zeste homolog 2 (Ezh2) restrains pathogenicity of NKT cells in the context of asthma-like lung disease. Methods: Numbers of invariant natural killer T (iNKT) 1, iNKT2, and iNKT17 cells and tissue distribution, cytokine production, lymphoid tissue localization, and transcriptional profiles of iNKT cells from wild-type and Ezh2 knockout (KO) iNKT mice were determined. The contribution of NKT cells to development of spontaneous and house dust mite-induced airways pathology, including airways hyperreactivity (AHR) to methacholine, was also assessed in wild-type, Ezh2 KO, and Ezh2 KO mice lacking NKT cells. Results: Ezh2 restrains development of pathogenic NKT cells, which induce spontaneous asthma-like disease in mice. Deletion of Ezh2 increased production of IL-4 and IL-13 and induced spontaneous AHR, lung inflammation, mucus production, and IgE. Increased IL-4 and IL-13 levels, AHR, lung inflammation, and IgE levels were all dependent on iNKT cells. In house dust mite-exposed animals Ezh2 KO resulted in enhanced AHR that was also dependent on iNKT cells. Conclusion: Ezh2 is a central regulator of iNKT pathogenicity and suppresses the ability of iNKT cells to induce asthma-like pathology.
MeSH term(s)	Animals ; Asthma/genetics ; Asthma/immunology ; Asthma/pathology ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Basic Helix-Loop-Helix Transcription Factors/immunology ; Enhancer of Zeste Homolog 2 Protein/genetics ; Enhancer of Zeste Homolog 2 Protein/immunology ; Immunoglobulin E/genetics ; Immunoglobulin E/immunology ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/pathology ; Interleukin-13/genetics ; Interleukin-13/immunology ; Interleukin-4/genetics ; Interleukin-4/immunology ; Lung/immunology ; Lung/pathology ; Mice ; Mice, Knockout ; Natural Killer T-Cells/immunology ; Natural Killer T-Cells/pathology ; Receptors, Aryl Hydrocarbon/genetics ; Receptors, Aryl Hydrocarbon/immunology
Chemical Substances	Ahr protein, mouse ; Basic Helix-Loop-Helix Transcription Factors ; Il4 protein, mouse ; Interleukin-13 ; Receptors, Aryl Hydrocarbon ; Interleukin-4 (207137-56-2) ; Immunoglobulin E (37341-29-0) ; Enhancer of Zeste Homolog 2 Protein (EC 2.1.1.43) ; Ezh2 protein, mouse (EC 2.1.1.43)
Language	English
Publishing date	2019-03-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2019.02.024
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