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Article ; Online: Arginine-dependent immune responses.

Martí I Líndez, Adrià-Arnau / Reith, Walter

Cellular and molecular life sciences : CMLS

2021 Volume 78, Issue 13, Page(s) 5303–5324

Abstract: A growing body of evidence indicates that, over the course of evolution of the immune system, arginine has been selected as a node for the regulation of immune responses. An appropriate supply of arginine has long been associated with the improvement of ... ...

Abstract	A growing body of evidence indicates that, over the course of evolution of the immune system, arginine has been selected as a node for the regulation of immune responses. An appropriate supply of arginine has long been associated with the improvement of immune responses. In addition to being a building block for protein synthesis, arginine serves as a substrate for distinct metabolic pathways that profoundly affect immune cell biology; especially macrophage, dendritic cell and T cell immunobiology. Arginine availability, synthesis, and catabolism are highly interrelated aspects of immune responses and their fine-tuning can dictate divergent pro-inflammatory or anti-inflammatory immune outcomes. Here, we review the organismal pathways of arginine metabolism in humans and rodents, as essential modulators of the availability of this semi-essential amino acid for immune cells. We subsequently review well-established and novel findings on the functional impact of arginine biosynthetic and catabolic pathways on the main immune cell lineages. Finally, as arginine has emerged as a molecule impacting on a plethora of immune functions, we integrate key notions on how the disruption or perversion of arginine metabolism is implicated in pathologies ranging from infectious diseases to autoimmunity and cancer.
MeSH term(s)	Animals ; Arginine/metabolism ; Communicable Diseases/immunology ; Communicable Diseases/metabolism ; Communicable Diseases/pathology ; Humans ; Immunity/immunology ; Neoplasms/immunology ; Neoplasms/metabolism ; Neoplasms/pathology
Chemical Substances	Arginine (94ZLA3W45F)
Language	English
Publishing date	2021-05-26
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-021-03828-4
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Article: Arginine-dependent immune responses

Martí i Líndez, Adrià-Arnau / Reith, Walter

Cellular and molecular life sciences. 2021 July, v. 78, no. 13

2021

Abstract	A growing body of evidence indicates that, over the course of evolution of the immune system, arginine has been selected as a node for the regulation of immune responses. An appropriate supply of arginine has long been associated with the improvement of immune responses. In addition to being a building block for protein synthesis, arginine serves as a substrate for distinct metabolic pathways that profoundly affect immune cell biology; especially macrophage, dendritic cell and T cell immunobiology. Arginine availability, synthesis, and catabolism are highly interrelated aspects of immune responses and their fine-tuning can dictate divergent pro-inflammatory or anti-inflammatory immune outcomes. Here, we review the organismal pathways of arginine metabolism in humans and rodents, as essential modulators of the availability of this semi-essential amino acid for immune cells. We subsequently review well-established and novel findings on the functional impact of arginine biosynthetic and catabolic pathways on the main immune cell lineages. Finally, as arginine has emerged as a molecule impacting on a plethora of immune functions, we integrate key notions on how the disruption or perversion of arginine metabolism is implicated in pathologies ranging from infectious diseases to autoimmunity and cancer.
Keywords	T-lymphocytes ; arginine ; autoimmunity ; biosynthesis ; catabolism ; dendritic cells ; evolution ; macrophages ; protein synthesis
Language	English
Dates of publication	2021-07
Size	p. 5303-5324.
Publishing place	Springer International Publishing
Document type	Article
Note	Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-021-03828-4
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Article ; Online: Regulation of Immunity by Butyrophilins.

Rhodes, David A / Reith, Walter / Trowsdale, John

Annual review of immunology

2016 Volume 34, Page(s) 151–172

Abstract: Butyrophilin molecules (commonly contracted to BTN), collectively take their name from the eponymous protein in cow's milk. They are considered to be members of the B7 family of costimulatory receptors, which includes B7.1 (CD80), B7.2 (CD86), and ... ...

Abstract	Butyrophilin molecules (commonly contracted to BTN), collectively take their name from the eponymous protein in cow's milk. They are considered to be members of the B7 family of costimulatory receptors, which includes B7.1 (CD80), B7.2 (CD86), and related molecules, such as PD-L1 (B7-H1, CD274), ICOS-L (CD275), and B7-H3 (CD276). These coreceptors modulate T cell responses upon antigen presentation by major histocompatibility complex and cognate αβ T cell receptor engagement. Molecules such as BTN3A1 (CD277), myelin oligodendrocyte glycoprotein, and mouse Skint1 and Btnl2, all members of the butyrophilin family, show greater structural and functional diversity than the canonical B7 receptors. Some butyrophilins mediate complex interactions between antigen-presenting cells and conventional αβ T cells, and others regulate the immune responses of specific γδ T cell subsets by mechanisms that have characteristics of both innate and adaptive immunity.
MeSH term(s)	Adaptive Immunity ; Animals ; Antigen-Presenting Cells/immunology ; B7 Antigens/metabolism ; Butyrophilins/immunology ; Butyrophilins/metabolism ; Cattle ; Humans ; Immunity, Innate ; Lymphocyte Activation ; Mice ; Milk/metabolism ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction ; T-Lymphocytes/immunology
Chemical Substances	B7 Antigens ; Butyrophilins ; Receptors, Antigen, T-Cell
Language	English
Publishing date	2016-01-11
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	604953-9
ISSN	1545-3278 ; 0732-0582
ISSN (online)	1545-3278
ISSN	0732-0582
DOI	10.1146/annurev-immunol-041015-055435
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Article: ComPLEXIN new targets for CIITA.

Reith, Walter

Nature immunology

2003 Volume 4, Issue 9, Page(s) 819–820

MeSH term(s)	Animals ; Dendritic Cells/immunology ; Histocompatibility Antigens Class II/immunology ; Mice ; Nerve Tissue Proteins/immunology ; Nuclear Proteins ; Receptors, Cell Surface/immunology ; T-Lymphocytes/immunology ; Trans-Activators/immunology ; Transcriptional Activation/immunology
Chemical Substances	Histocompatibility Antigens Class II ; MHC class II transactivator protein ; Nerve Tissue Proteins ; Nuclear Proteins ; Plxna1 protein, mouse ; Receptors, Cell Surface ; Trans-Activators
Language	English
Publishing date	2003-09
Publishing country	United States
Document type	Comment ; News
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/ni0903-819
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Article ; Online: Toll-like receptor 4 inhibition prevents autoimmune diabetes in NOD mice.

Alibashe-Ahmed, Mohamed / Brioudes, Estelle / Reith, Walter / Bosco, Domenico / Berney, Thierry

Scientific reports

2019 Volume 9, Issue 1, Page(s) 19350

Abstract: TLR4 is a transmembrane receptor of the innate immune system that recognizes LPS from gram-negative bacteria. Its stimulation induces pro-inflammatory responses and modulates adaptive immunity. Our aim is to determine the role of TLR4 in the activation ... ...

Abstract	TLR4 is a transmembrane receptor of the innate immune system that recognizes LPS from gram-negative bacteria. Its stimulation induces pro-inflammatory responses and modulates adaptive immunity. Our aim is to determine the role of TLR4 in the activation and proliferation of T lymphocytes in the onset of autoimmune diabetes, using the non-obese diabetic (NOD) mouse model. Antigen-specific activation and proliferation of diabetogenic T cells were assessed in vitro by Carboxyfluorescein succinimidyl ester (CFSE) dilution, in presence of vehicle or CLI-095, a cyclohexene derivative that inhibits TLR4 signaling. NOD mice were treated with vehicle or CLI-095 and sacrificed either before or after the onset of autoimmune diabetes. T lymphocyte activation and proliferation were evaluated in treated and control mice. Insulitis was analyzed by histology and diabetes incidence was determined in treated and control mice. Our results demonstrate that TLR4 blockade decreases CD4+ T lymphocyte activation and auto-antigen-specific proliferation both in vitro and in vivo, decreases the infiltrative insulitis and finally prevents the onset of spontaneous diabetes. Taken together, our data demonstrate that TLR4 signaling contributes to the development and maintenance of autoimmune diabetes. The immunomodulatory effect of CLI-095 could be part of a preventive strategy targeting patients at risk for type 1 diabetes.
MeSH term(s)	Adoptive Transfer ; Animals ; CD3 Complex/metabolism ; CD4-Positive T-Lymphocytes/cytology ; CD4-Positive T-Lymphocytes/drug effects ; CD4-Positive T-Lymphocytes/immunology ; Cell Proliferation/drug effects ; Diabetes Mellitus, Type 1/prevention & control ; Epitopes/metabolism ; Female ; Lymphocyte Activation/drug effects ; Lymphocyte Activation/immunology ; Mice, Inbred NOD ; Receptors, Antigen, T-Cell/metabolism ; Sulfonamides/pharmacology ; Toll-Like Receptor 4/antagonists & inhibitors ; Toll-Like Receptor 4/metabolism
Chemical Substances	CD3 Complex ; Epitopes ; Receptors, Antigen, T-Cell ; Sulfonamides ; Toll-Like Receptor 4 ; ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate
Language	English
Publishing date	2019-12-18
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/s41598-019-55521-z
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Article ; Online: A Multi-Omics Approach Reveals Features That Permit Robust and Widespread Regulation of IFN-Inducible Antiviral Effectors.

Göczi, Loránd / Csumita, Mária / Horváth, Attila / Nagy, Gergely / Póliska, Szilárd / Pigni, Matteo / Thelemann, Christoph / Dániel, Bence / Mianesaz, Hamidreza / Varga, Tamás / Sen, Kaushik / Raghav, Sunil K / Schoggins, John W / Nagy, Laszlo / Acha-Orbea, Hans / Meissner, Felix / Reith, Walter / Széles, Lajos

Journal of immunology (Baltimore, Md. : 1950)

2022 Volume 209, Issue 10, Page(s) 1930–1941

Abstract: The antiviral state, an initial line of defense against viral infection, is established by a set of IFN-stimulated genes (ISGs) encoding antiviral effector proteins. The effector ISGs are transcriptionally regulated by type I IFNs mainly via activation ... ...

Abstract	The antiviral state, an initial line of defense against viral infection, is established by a set of IFN-stimulated genes (ISGs) encoding antiviral effector proteins. The effector ISGs are transcriptionally regulated by type I IFNs mainly via activation of IFN-stimulated gene factor 3 (ISGF3). In this study, the regulatory elements of effector ISGs were characterized to determine the (epi)genetic features that enable their robust induction by type I IFNs in multiple cell types. We determined the location of regulatory elements, the DNA motifs, the occupancy of ISGF3 subunits (IRF9, STAT1, and STAT2) and other transcription factors, and the chromatin accessibility of 37 effector ISGs in murine dendritic cells. The IFN-stimulated response element (ISRE) and its tripartite version occurred most frequently in the regulatory elements of effector ISGs than in any other tested ISG subsets. Chromatin accessibility at their promoter regions was similar to most other ISGs but higher than at the promoters of inflammation-related cytokines, which were used as a reference gene set. Most effector ISGs (81.1%) had at least one ISGF3 binding region proximal to the transcription start site (TSS), and only a subset of effector ISGs (24.3%) was associated with three or more ISGF3 binding regions. The IRF9 signals were typically higher, and ISRE motifs were "stronger" (more similar to the canonical sequence) in TSS-proximal versus TSS-distal regulatory regions. Moreover, most TSS-proximal regulatory regions were accessible before stimulation in multiple cell types. Our results indicate that "strong" ISRE motifs and universally accessible promoter regions that permit robust, widespread induction are characteristic features of effector ISGs.
MeSH term(s)	Animals ; Mice ; Antiviral Restriction Factors ; Chromatin/genetics ; Nucleotide Motifs ; Promoter Regions, Genetic/genetics ; Response Elements/genetics ; Interferons/metabolism
Chemical Substances	Antiviral Restriction Factors ; Chromatin ; Interferons (9008-11-1)
Language	English
Publishing date	2022-11-24
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.2200363
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Article ; Online: Novel Mutation in the Class II Transactivator Associated with Immunodeficiency and Autoimmunity.

Ahmed, Aisha / Reith, Walter / Puck, Jennifer M / Cheng, Laurence E

Journal of clinical immunology

2015 Volume 35, Issue 6, Page(s) 521–522

MeSH term(s)	Adolescent ; CD4-Positive T-Lymphocytes/immunology ; Child ; Codon, Nonsense/genetics ; Consanguinity ; Female ; Genotype ; Granulocyte Colony-Stimulating Factor/administration & dosage ; HLA-DR Antigens/genetics ; HLA-DR Antigens/metabolism ; Humans ; Immunoglobulins, Intravenous/administration & dosage ; Infant ; Nuclear Proteins/genetics ; Pneumocystis carinii/genetics ; Pneumocystis carinii/immunology ; Trans-Activators/genetics
Chemical Substances	Codon, Nonsense ; HLA-DR Antigens ; Immunoglobulins, Intravenous ; MHC class II transactivator protein ; Nuclear Proteins ; Trans-Activators ; Granulocyte Colony-Stimulating Factor (143011-72-7)
Language	English
Publishing date	2015-08
Publishing country	Netherlands
Document type	Case Reports ; Letter
ZDB-ID	779361-3
ISSN	1573-2592 ; 0271-9142
ISSN (online)	1573-2592
ISSN	0271-9142
DOI	10.1007/s10875-015-0183-z
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Article ; Online: Macrophage migration inhibitory factor regulates TLR4 expression and modulates TCR/CD3-mediated activation in CD4+ T lymphocytes.

Alibashe-Ahmed, Mohamed / Roger, Thierry / Serre-Beinier, Veronique / Berishvili, Ekaterine / Reith, Walter / Bosco, Domenico / Berney, Thierry

Scientific reports

2019 Volume 9, Issue 1, Page(s) 9380

Abstract: Toll-like receptor 4 (TLR4) is involved in CD4+ T lymphocyte-mediated pathologies. Here, we demonstrate that CD4+ T lymphocytes express functional TLR4 that contributes to their activation, proliferation and cytokine secretion. In addition, we ... ...

Abstract	Toll-like receptor 4 (TLR4) is involved in CD4+ T lymphocyte-mediated pathologies. Here, we demonstrate that CD4+ T lymphocytes express functional TLR4 that contributes to their activation, proliferation and cytokine secretion. In addition, we demonstrate that TLR4-induced responses are mediated by macrophage migration inhibitory factor (MIF), a pro-inflammatory cytokine. We also demonstrate that MIF regulates suboptimal TCR/CD3-mediated activation of T lymphocytes. On one hand, MIF prevents excessive TCR/CD3-mediated activation of CD4+ T lymphocytes under suboptimal stimulation conditions and, on the other hand, MIF enables activated CD4+ T lymphocytes to sense their microenvironment and adapt their effector response through TLR4. Therefore, MIF appears to be a major regulator of the activation of CD4+ T lymphocytes and the intensity of their effector response. TLR4-mediated activation is thus an important process for T cell-mediated immunity.
MeSH term(s)	Animals ; Biomarkers ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/metabolism ; Gene Expression Regulation ; Immunomodulation ; Immunophenotyping ; Intramolecular Oxidoreductases/metabolism ; Lipopolysaccharides/immunology ; Lymphocyte Activation/genetics ; Lymphocyte Activation/immunology ; Macrophage Migration-Inhibitory Factors/metabolism ; Macrophages/immunology ; Macrophages/metabolism ; Mice ; Receptor-CD3 Complex, Antigen, T-Cell/metabolism ; Toll-Like Receptor 4/genetics ; Toll-Like Receptor 4/metabolism
Chemical Substances	Biomarkers ; Lipopolysaccharides ; Macrophage Migration-Inhibitory Factors ; Receptor-CD3 Complex, Antigen, T-Cell ; Tlr4 protein, mouse ; Toll-Like Receptor 4 ; Intramolecular Oxidoreductases (EC 5.3.-) ; Mif protein, mouse (EC 5.3.2.1)
Language	English
Publishing date	2019-06-28
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/s41598-019-45260-6
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Article ; Online: Specific enhancer selection by IRF3, IRF5 and IRF9 is determined by ISRE half-sites, 5' and 3' flanking bases, collaborating transcription factors and the chromatin environment in a combinatorial fashion.

Csumita, Mária / Csermely, Attila / Horvath, Attila / Nagy, Gergely / Monori, Fanny / Göczi, Loránd / Orbea, Hans-Acha / Reith, Walter / Széles, Lajos

Nucleic acids research

2019 Volume 48, Issue 2, Page(s) 589–604

Abstract: IRF3, IRF5 and IRF9 are transcription factors, which play distinct roles in the regulation of antiviral and inflammatory responses. The determinants that mediate IRF-specific enhancer selection are not fully understood. To uncover regions occupied ... ...

Abstract	IRF3, IRF5 and IRF9 are transcription factors, which play distinct roles in the regulation of antiviral and inflammatory responses. The determinants that mediate IRF-specific enhancer selection are not fully understood. To uncover regions occupied predominantly by IRF3, IRF5 or IRF9, we performed ChIP-seq experiments in activated murine dendritic cells. The identified regions were analysed with respect to the enrichment of DNA motifs, the interferon-stimulated response element (ISRE) and ISRE half-site variants, and chromatin accessibility. Using a machine learning method, we investigated the predictability of IRF-dominance. We found that IRF5-dominant regions differed fundamentally from the IRF3- and IRF9-dominant regions: ISREs were rare, while the NFKB motif and special ISRE half-sites, such as 5'-GAGA-3' and 5'-GACA-3', were enriched. IRF3- and IRF9-dominant regions were characterized by the enriched ISRE motif and lower frequency of accessible chromatin. Enrichment analysis and the machine learning method uncovered the features that favour IRF3 or IRF9 dominancy (e.g. a tripartite form of ISRE and motifs for NF-κB for IRF3, and the GAS motif and certain ISRE variants for IRF9). This study contributes to our understanding of how IRF members, which bind overlapping sets of DNA sequences, can initiate signal-dependent responses without activating superfluous or harmful programmes.
MeSH term(s)	Animals ; Cell Line ; Chromatin/genetics ; Dendritic Cells/metabolism ; Enhancer Elements, Genetic/genetics ; Gene Expression Regulation ; Humans ; Interferon Regulatory Factor-3/genetics ; Interferon Regulatory Factors/genetics ; Interferon-Stimulated Gene Factor 3, gamma Subunit/genetics ; Machine Learning ; Mice ; NF-kappa B/genetics ; Nucleotide Motifs/genetics ; Principal Component Analysis ; Response Elements/genetics ; Transcription Factors/genetics
Chemical Substances	Chromatin ; IRF3 protein, human ; IRF5 protein, human ; IRF9 protein, human ; Interferon Regulatory Factor-3 ; Interferon Regulatory Factors ; Interferon-Stimulated Gene Factor 3, gamma Subunit ; NF-kappa B ; Transcription Factors
Language	English
Publishing date	2019-11-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkz1112
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Article ; Online: New dimensions of CIITA.

Reith, Walter / Boss, Jeremy M

Nature immunology

2008 Volume 9, Issue 7, Page(s) 713–714

MeSH term(s)	Animals ; Gene Expression ; Gene Expression Regulation ; Humans ; Nuclear Proteins/genetics ; Promoter Regions, Genetic ; Trans-Activators/genetics
Chemical Substances	MHC class II transactivator protein ; Nuclear Proteins ; Trans-Activators
Language	English
Publishing date	2008-06-17
Publishing country	United States
Document type	Comment ; News
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/ni0708-713
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