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Article ; Online: Tim-3 adaptor protein Bat3 is a molecular checkpoint of T cell terminal differentiation and exhaustion.

Zhu, Chen / Dixon, Karen O / Newcomer, Kathleen / Gu, Guangxiang / Xiao, Sheng / Zaghouani, Sarah / Schramm, Markus A / Wang, Chao / Zhang, Huiyuan / Goto, Kouichiro / Christian, Elena / Rangachari, Manu / Rosenblatt-Rosen, Orit / Okada, Hitoshi / Mak, Tak / Singer, Meromit / Regev, Aviv / Kuchroo, Vijay

Science advances

2021 Volume 7, Issue 18

Abstract: T cell exhaustion has been associated with poor prognosis in persistent viral infection and cancer. Conversely, in the context of autoimmunity, T cell exhaustion has been favorably correlated with long-term clinical outcome. Understanding the development ...

Abstract	T cell exhaustion has been associated with poor prognosis in persistent viral infection and cancer. Conversely, in the context of autoimmunity, T cell exhaustion has been favorably correlated with long-term clinical outcome. Understanding the development of exhaustion in autoimmune settings may provide underlying principles that can be exploited to quell autoreactive T cells. Here, we demonstrate that the adaptor molecule Bat3 acts as a molecular checkpoint of T cell exhaustion, with deficiency of Bat3 promoting a profound exhaustion phenotype, suppressing autoreactive T cell-mediated neuroinflammation. Mechanistically, Bat3 acts as a critical mTORC2 inhibitor to suppress Akt function. As a result, Bat3 deficiency leads to increased Akt activity and FoxO1 phosphorylation, indirectly promoting
Language	English
Publishing date	2021-04-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.abd2710
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Article ; Online: B-cell-specific checkpoint molecules that regulate anti-tumour immunity.

Bod, Lloyd / Kye, Yoon-Chul / Shi, Jingwen / Torlai Triglia, Elena / Schnell, Alexandra / Fessler, Johannes / Ostrowski, Stephen M / Von-Franque, Max Y / Kuchroo, Juhi R / Barilla, Rocky M / Zaghouani, Sarah / Christian, Elena / Delorey, Toni Marie / Mohib, Kanishka / Xiao, Sheng / Slingerland, Nadine / Giuliano, Christopher J / Ashenberg, Orr / Li, Zhaorong /

Rothstein, David M / Fisher, David E / Rozenblatt-Rosen, Orit / Sharpe, Arlene H / Quintana, Francisco J / Apetoh, Lionel / Regev, Aviv / Kuchroo, Vijay K

Nature

2023 Volume 619, Issue 7969, Page(s) 348–356

Abstract: The role of B cells in anti-tumour immunity is still debated and, accordingly, immunotherapies have focused on targeting T and natural killer cells to inhibit tumour ... ...

Abstract	The role of B cells in anti-tumour immunity is still debated and, accordingly, immunotherapies have focused on targeting T and natural killer cells to inhibit tumour growth
MeSH term(s)	Animals ; Mice ; B-Lymphocytes/cytology ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; Lymphocyte Activation ; Melanoma/immunology ; Melanoma/pathology ; Melanoma/prevention & control ; T-Lymphocytes/cytology ; T-Lymphocytes/immunology ; Flow Cytometry ; Melanoma, Experimental/immunology ; Melanoma, Experimental/pathology ; Lymph Nodes/cytology ; Lymph Nodes/immunology ; Antigen Presentation ; Receptors, Antigen, B-Cell/genetics ; Single-Cell Gene Expression Analysis ; Tumor Burden ; Interferon Type I
Chemical Substances	Havcr1 protein, mouse ; Lag3 protein, mouse ; T cell Ig and ITIM domain protein, mouse ; Receptors, Antigen, B-Cell ; Interferon Type I
Language	English
Publishing date	2023-06-21
Publishing country	England
Document type	Journal Article
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-023-06231-0
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Article: Metabolic modeling of single Th17 cells reveals regulators of autoimmunity

Wagner, Allon / Wang, Chao / Fessler, Johannes / DeTomaso, David / Avila-Pacheco, Julian / Kaminski, James / Zaghouani, Sarah / Christian, Elena / Thakore, Pratiksha / Schellhaass, Brandon / Akama-Garren, Elliot / Pierce, Kerry / Singh, Vasundhara / Ron-Harel, Noga / Douglas, Vivian Paraskevi / Bod, Lloyd / Schnell, Alexandra / Puleston, Daniel / Sobel, Raymond A. /

Haigis, Marcia / Pearce, Erika L. / Soleimani, Manoocher / Clish, Clary / Regev, Aviv / Kuchroo, Vijay K. / Yosef, Nir

Cell. 2021 Aug. 05, v. 184, no. 16

2021

Abstract: Metabolism is a major regulator of immune cell function, but it remains difficult to study the metabolic status of individual cells. Here, we present Compass, an algorithm to characterize cellular metabolic states based on single-cell RNA sequencing and ... ...

Abstract	Metabolism is a major regulator of immune cell function, but it remains difficult to study the metabolic status of individual cells. Here, we present Compass, an algorithm to characterize cellular metabolic states based on single-cell RNA sequencing and flux balance analysis. We applied Compass to associate metabolic states with T helper 17 (Th17) functional variability (pathogenic potential) and recovered a metabolic switch between glycolysis and fatty acid oxidation, akin to known Th17/regulatory T cell (Treg) differences, which we validated by metabolic assays. Compass also predicted that Th17 pathogenicity was associated with arginine and downstream polyamine metabolism. Indeed, polyamine-related enzyme expression was enhanced in pathogenic Th17 and suppressed in Treg cells. Chemical and genetic perturbation of polyamine metabolism inhibited Th17 cytokines, promoted Foxp3 expression, and remodeled the transcriptome and epigenome of Th17 cells toward a Treg-like state. In vivo perturbations of the polyamine pathway altered the phenotype of encephalitogenic T cells and attenuated tissue inflammation in CNS autoimmunity.
Keywords	CD4-positive T-lymphocytes ; RNA ; algorithms ; arginine ; autoimmunity ; beta oxidation ; cytokines ; enzymes ; epigenome ; glycolysis ; inflammation ; pathogenicity ; phenotype ; polyamines ; transcriptome
Language	English
Dates of publication	2021-0805
Size	p. 4168-4185.e21.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2021.05.045
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Article ; Online: Metabolic modeling of single Th17 cells reveals regulators of autoimmunity.

Haigis, Marcia / Pearce, Erika L / Soleimani, Manoocher / Clish, Clary / Regev, Aviv / Kuchroo, Vijay K / Yosef, Nir

Cell

2021 Volume 184, Issue 16, Page(s) 4168–4185.e21

Abstract	Metabolism is a major regulator of immune cell function, but it remains difficult to study the metabolic status of individual cells. Here, we present Compass, an algorithm to characterize cellular metabolic states based on single-cell RNA sequencing and flux balance analysis. We applied Compass to associate metabolic states with T helper 17 (Th17) functional variability (pathogenic potential) and recovered a metabolic switch between glycolysis and fatty acid oxidation, akin to known Th17/regulatory T cell (Treg) differences, which we validated by metabolic assays. Compass also predicted that Th17 pathogenicity was associated with arginine and downstream polyamine metabolism. Indeed, polyamine-related enzyme expression was enhanced in pathogenic Th17 and suppressed in Treg cells. Chemical and genetic perturbation of polyamine metabolism inhibited Th17 cytokines, promoted Foxp3 expression, and remodeled the transcriptome and epigenome of Th17 cells toward a Treg-like state. In vivo perturbations of the polyamine pathway altered the phenotype of encephalitogenic T cells and attenuated tissue inflammation in CNS autoimmunity.
MeSH term(s)	Acetyltransferases/metabolism ; Adenosine Triphosphate/metabolism ; Aerobiosis/drug effects ; Algorithms ; Animals ; Autoimmunity/drug effects ; Autoimmunity/immunology ; Chromatin/metabolism ; Citric Acid Cycle/drug effects ; Cytokines/metabolism ; Eflornithine/pharmacology ; Encephalomyelitis, Autoimmune, Experimental/metabolism ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Epigenome ; Fatty Acids/metabolism ; Glycolysis/drug effects ; Jumonji Domain-Containing Histone Demethylases/metabolism ; Mice, Inbred C57BL ; Mitochondrial Membrane Transport Proteins/metabolism ; Models, Biological ; Oxidation-Reduction/drug effects ; Putrescine/metabolism ; Single-Cell Analysis ; T-Lymphocytes, Regulatory/drug effects ; T-Lymphocytes, Regulatory/immunology ; Th17 Cells/drug effects ; Th17 Cells/immunology ; Transcriptome/genetics ; Mice
Chemical Substances	Chromatin ; Cytokines ; Fatty Acids ; Mitochondrial Membrane Transport Proteins ; Adenosine Triphosphate (8L70Q75FXE) ; Jumonji Domain-Containing Histone Demethylases (EC 1.14.11.-) ; Kdm6b protein, mouse (EC 1.5.-) ; Acetyltransferases (EC 2.3.1.-) ; diamine N-acetyltransferase (EC 2.3.1.57) ; Putrescine (V10TVZ52E4) ; Eflornithine (ZQN1G5V6SR)
Language	English
Publishing date	2021-07-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2021.05.045
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Article ; Online: Corrigendum: An IL-27/NFIL3 signalling axis drives Tim-3 and IL-10 expression and T-cell dysfunction.

Zhu, Chen / Sakuishi, Kaori / Xiao, Sheng / Sun, Zhiyi / Zaghouani, Sarah / Gu, Guangxiang / Wang, Chao / Tan, Dewar J / Wu, Chuan / Rangachari, Manu / Pertel, Thomas / Jin, Hyun-Tak / Ahmed, Rafi / Anderson, Ana C / Kuchroo, Vijay K

Nature communications

2015 Volume 6, Page(s) 7657

Language	English
Publishing date	2015-07-08
Publishing country	England
Document type	Published Erratum
ISSN	2041-1723
ISSN (online)	2041-1723
DOI	10.1038/ncomms8657
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Article ; Online: An IL-27/NFIL3 signalling axis drives Tim-3 and IL-10 expression and T-cell dysfunction.

Nature communications

2015 Volume 6, Page(s) 6072

Abstract: The inhibitory receptor T-cell immunoglobulin and mucin domain-3 (Tim-3) has emerged as a critical regulator of the T-cell dysfunction that develops in chronic viral infections and cancers. However, little is known regarding the signalling pathways that ... ...

Abstract	The inhibitory receptor T-cell immunoglobulin and mucin domain-3 (Tim-3) has emerged as a critical regulator of the T-cell dysfunction that develops in chronic viral infections and cancers. However, little is known regarding the signalling pathways that drive Tim-3 expression. Here, we demonstrate that interleukin (IL)-27 induces nuclear factor, interleukin 3 regulated (NFIL3), which promotes permissive chromatin remodelling of the Tim-3 locus and induces Tim-3 expression together with the immunosuppressive cytokine IL-10. We further show that the IL-27/NFIL3 signalling axis is crucial for the induction of Tim-3 in vivo. IL-27-conditioned T helper 1 cells exhibit reduced effector function and are poor mediators of intestinal inflammation. This inhibitory effect is NFIL3 dependent. In contrast, tumour-infiltrating lymphocytes from IL-27R(-/-) mice exhibit reduced NFIL3, less Tim-3 expression and failure to develop dysfunctional phenotype, resulting in better tumour growth control. Thus, our data identify an IL-27/NFIL3 signalling axis as a key regulator of effector T-cell responses via induction of Tim-3, IL-10 and T-cell dysfunction.
MeSH term(s)	Animals ; Basic-Leucine Zipper Transcription Factors/metabolism ; CD4-Positive T-Lymphocytes/immunology ; Chromatin/metabolism ; Clonal Anergy/immunology ; Gastrointestinal Tract/pathology ; Hepatitis A Virus Cellular Receptor 2 ; Inflammation/immunology ; Inflammation/pathology ; Interleukin-10/metabolism ; Interleukin-27/deficiency ; Interleukin-27/metabolism ; Mice, Inbred C57BL ; Neoplasms/immunology ; Neoplasms/pathology ; Receptors, Virus/metabolism ; STAT1 Transcription Factor/metabolism ; STAT3 Transcription Factor/metabolism ; Signal Transduction ; T-Box Domain Proteins/metabolism
Chemical Substances	Basic-Leucine Zipper Transcription Factors ; Chromatin ; Havcr2 protein, mouse ; Hepatitis A Virus Cellular Receptor 2 ; Interleukin-27 ; Nfil3 protein, mouse ; Receptors, Virus ; STAT1 Transcription Factor ; STAT3 Transcription Factor ; T-Box Domain Proteins ; T-box transcription factor TBX21 ; Interleukin-10 (130068-27-8)
Language	English
Publishing date	2015-01-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2041-1723
ISSN (online)	2041-1723
DOI	10.1038/ncomms7072
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Article ; Online: Recovery from overt type 1 diabetes ensues when immune tolerance and β-cell formation are coupled with regeneration of endothelial cells in the pancreatic islets.

Wan, Xiaoxiao / Guloglu, F Betul / Vanmorlan, Amie M / Rowland, Linda M / Zaghouani, Sarah / Cascio, Jason A / Dhakal, Mermagya / Hoeman, Christine M / Zaghouani, Habib

Diabetes

2013 Volume 62, Issue 8, Page(s) 2879–2889

Abstract: Immune modulation of pancreatic inflammation induces recovery from type 1 diabetes (T1D), but remission was not durable, perhaps because of an inability to sustain the formation and function of new pancreatic β-cells. We have previously shown that Ig- ... ...

Abstract	Immune modulation of pancreatic inflammation induces recovery from type 1 diabetes (T1D), but remission was not durable, perhaps because of an inability to sustain the formation and function of new pancreatic β-cells. We have previously shown that Ig-GAD2, carrying GAD 206-220 peptide, induced in hyperglycemic mice immune modulation that was able to control pancreatic inflammation, stimulate β-cell regeneration, and prevent T1D progression. Herein, we show that the same Ig-GAD2 regimen given to mice with overt T1D was unable to reverse the course of disease despite eradication of Th1 and Th17 cells from the pancreas. However, the regimen was able to sustain recovery from T1D when Ig-GAD2 was accompanied with transfer of bone marrow (BM) cells from healthy donors. Interestingly, alongside immune modulation, there was concomitant formation of new β-cells and endothelial cells (ECs) in the pancreas. The new β-cells were of host origin while the donor BM cells gave rise to the ECs. Moreover, transfer of purified BM endothelial progenitors instead of whole BM cells sustained both β-cell and EC formation and reversal of diabetes. Thus, overcoming T1D requires both immune modulation and repair of the islet vascular niche to preserve newly formed β-cells.
MeSH term(s)	Animals ; B-Lymphocytes/immunology ; Bone Marrow Transplantation ; Diabetes Mellitus, Type 1/immunology ; Disease Progression ; Endothelial Cells/immunology ; Immune Tolerance/immunology ; Immunoglobulins/immunology ; Inflammation/immunology ; Islets of Langerhans/immunology ; Mice ; Mice, Inbred NOD ; Regeneration
Chemical Substances	Immunoglobulins
Language	English
Publishing date	2013-05-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db12-1281
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Article ; Online: Antigen-specific effector CD4 T lymphocytes school lamina propria dendritic cells to transfer innate tolerance.

Cascio, Jason A / Haymaker, Cara L / Divekar, Rohit D / Zaghouani, Sarah / Khairallah, Marie-Therese / Wan, Xiaoxiao / Rowland, Linda M / Dhakal, Mermagya / Chen, Weirong / Zaghouani, Habib

Journal of immunology (Baltimore, Md. : 1950)

2013 Volume 190, Issue 12, Page(s) 6004–6014

Abstract: Dendritic cells (DCs) have been shown to play a major role in oral tolerance, and this function has been associated with their ability to produce anti-inflammatory cytokines and to induce suppressive regulatory T cells. In this study, we demonstrate that ...

Abstract	Dendritic cells (DCs) have been shown to play a major role in oral tolerance, and this function has been associated with their ability to produce anti-inflammatory cytokines and to induce suppressive regulatory T cells. In this study, we demonstrate that upon oral administration of Ag, lamina propia (LP) DCs engage specific T cells and acquire a novel mechanism by which they transfer tolerance against diverse T cell specificities. Indeed, when Ig-myelin oligodendrocyte glycoprotein (MOG) carrying the MOG(35-55) epitope was orally administered into either T cell-sufficient or -deficient mice, only the T cell-sufficient hosts yielded CD8α(+) and CD8α(-) LP DCs that were able to transfer tolerance to a variety of MHC class II-restricted effector T cells. Surprisingly, these LP DCs upregulated programmed cell death ligand 1 during the initial interaction with MOG-specific T cells and used this inhibitory molecule to suppress activation of T cells regardless of Ag specificity. Furthermore, oral Ig-MOG was able to overcome experimental autoimmune encephalomyelitis induced with CNS homogenate, indicating that the DCs are able to modulate disease involving diverse T cell specificities. This previously unrecognized attribute potentiates DCs against autoimmunity.
MeSH term(s)	Administration, Oral ; Adoptive Transfer ; Animals ; Autoantigens/immunology ; Autoimmunity/immunology ; CD4-Positive T-Lymphocytes/immunology ; Cell Separation ; Dendritic Cells/immunology ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Enzyme-Linked Immunosorbent Assay ; Flow Cytometry ; Immune Tolerance/immunology ; Immunity, Innate/immunology ; Immunity, Mucosal/immunology ; Lymphocyte Activation/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mucous Membrane/immunology ; Myelin-Oligodendrocyte Glycoprotein/administration & dosage ; Myelin-Oligodendrocyte Glycoprotein/immunology ; Peptide Fragments/administration & dosage ; Peptide Fragments/immunology
Chemical Substances	Autoantigens ; Myelin-Oligodendrocyte Glycoprotein ; Peptide Fragments ; myelin oligodendrocyte glycoprotein (35-55)
Language	English
Publishing date	2013-05-17
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.1203552
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Article ; Online: Bone marrow-derived IL-13Rα1-positive thymic progenitors are restricted to the myeloid lineage.

Haymaker, Cara L / Guloglu, F Betul / Cascio, Jason A / Hardaway, John C / Dhakal, Mermagya / Wan, Xiaoxiao / Hoeman, Christine M / Zaghouani, Sarah / Rowland, Linda M / Tartar, Danielle M / VanMorlan, Amie M / Zaghouani, Habib

Journal of immunology (Baltimore, Md. : 1950)

2012 Volume 188, Issue 7, Page(s) 3208–3216

Abstract: The earliest thymic progenitors (ETPs) were recently shown to give rise to both lymphoid and myeloid cells. Whereas the majority of ETPs are derived from IL-7Rα-positive cells and give rise exclusively to T cells, the origin of the myeloid cells remains ... ...

Abstract	The earliest thymic progenitors (ETPs) were recently shown to give rise to both lymphoid and myeloid cells. Whereas the majority of ETPs are derived from IL-7Rα-positive cells and give rise exclusively to T cells, the origin of the myeloid cells remains undefined. In this study, we show both in vitro and in vivo that IL-13Rα1(+) ETPs yield myeloid cells with no potential for maturation into T cells, whereas IL-13Rα1(-) ETPs lack myeloid potential. Moreover, transfer of lineage-negative IL-13Rα1(+) bone marrow stem cells into IL-13Rα1-deficient mice reconstituted thymic IL-13Rα1(+) myeloid ETPs. Myeloid cells or macrophages in the thymus are regarded as phagocytic cells whose function is to clear apoptotic debris generated during T cell development. However, the myeloid cells derived from IL-13Rα1(+) ETPs were found to perform Ag-presenting functions. Thus, IL-13Rα1 defines a new class of myeloid restricted ETPs yielding APCs that could contribute to development of T cells and the control of immunity and autoimmunity.
MeSH term(s)	Animals ; Antigen-Presenting Cells/chemistry ; Antigen-Presenting Cells/cytology ; Antigen-Presenting Cells/drug effects ; Antigen-Presenting Cells/immunology ; Antigens, Differentiation/analysis ; Bone Marrow Cells/chemistry ; Bone Marrow Cells/classification ; Cell Lineage ; Cell Movement ; Cells, Cultured ; Female ; Gene Knock-In Techniques ; Granulocyte-Macrophage Progenitor Cells/chemistry ; Granulocyte-Macrophage Progenitor Cells/cytology ; Granulocyte-Macrophage Progenitor Cells/drug effects ; Granulocyte-Macrophage Progenitor Cells/immunology ; Interleukin-13/pharmacology ; Interleukin-13 Receptor alpha1 Subunit/analysis ; Interleukin-13 Receptor alpha1 Subunit/deficiency ; Interleukin-13 Receptor alpha1 Subunit/genetics ; Lymphocytes, Null/cytology ; Lymphopoiesis ; Male ; Mice ; Mice, Congenic ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Myelopoiesis ; Sequence Deletion ; T-Lymphocytes/cytology ; Thymus Gland/cytology
Chemical Substances	Antigens, Differentiation ; Il13ra1 protein, mouse ; Interleukin-13 ; Interleukin-13 Receptor alpha1 Subunit
Language	English
Publishing date	2012-02-20
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.1103316
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