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Book ; Online ; Conference proceedings: Proceedings of ICI Milan 2013

Rosa, Francesca Di / Weiss, Jerrold / Meuer, Stefan Carl Wilhelm / Schwartz, Ronald H. / Zanovello, Paola / Smith, Kendall A / Dieli, Francesco / Martini, Alberto / Grice, Elizabeth Anne / Riccardi, Carlo

2014

Abstract: This Research Topic covers all of the major lectures and symposia addresses delivered by invited speakers at the 2013 International Congress in Immunology (ICI) at Milan, Italy, August 22-27, ... ...

Abstract	This Research Topic covers all of the major lectures and symposia addresses delivered by invited speakers at the 2013 International Congress in Immunology (ICI) at Milan, Italy, August 22-27, 2013
Keywords	Immunologic diseases. Allergy ; Medicine (General)
Size	1 electronic resource (196 p.)
Publisher	Frontiers Media SA
Document type	Book ; Online ; Conference proceedings
Note	English ; Open Access
HBZ-ID	HT020090987
ISBN	9782889193387 ; 2889193381
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article ; Online: Historical overview of immunological tolerance.

Schwartz, Ronald H

Cold Spring Harbor perspectives in biology

2012 Volume 4, Issue 4, Page(s) a006908

Abstract: A fundamental property of the immune system is its ability to mediate self-defense with a minimal amount of collateral damage to the host. The system uses several different mechanisms to achieve this goal, which is collectively referred to as the " ... ...

Abstract	A fundamental property of the immune system is its ability to mediate self-defense with a minimal amount of collateral damage to the host. The system uses several different mechanisms to achieve this goal, which is collectively referred to as the "process of immunological tolerance." This article provides an introductory historical overview to these various mechanisms, which are discussed in greater detail throughout this collection, and then briefly describes what happens when this process fails, a state referred to as "autoimmunity."
MeSH term(s)	Humans ; Immune Tolerance
Language	English
Publishing date	2012-04-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Review
ISSN	1943-0264
ISSN (online)	1943-0264
DOI	10.1101/cshperspect.a006908
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Article: Natural regulatory T cells and self-tolerance.

Schwartz, Ronald H

Nature immunology

2005 Volume 6, Issue 4, Page(s) 327–330

Abstract: The adaptive immune system allows individual organisms to mount defensive reactions against unanticipated pathogens by developmentally creating a diverse repertoire of clonally distributed receptors capable of recognizing a multitude of antigens and then ...

Abstract	The adaptive immune system allows individual organisms to mount defensive reactions against unanticipated pathogens by developmentally creating a diverse repertoire of clonally distributed receptors capable of recognizing a multitude of antigens and then expanding as effector cell populations those that can recognize molecules from the pathogens. To function properly, the system must deal with the problem of randomly generated receptors that can recognize self components. Most solutions to this self-tolerance problem are cell intrinsic and involve the deletion or inactivation of autoreactive cells. However, an extrinsic form of dominant tolerance has been demonstrated that takes the form of CD4(+) regulatory T cells. This perspective discusses why such a mechanism might have evolved and the problems it presents for self-non-self discrimination.
MeSH term(s)	Animals ; Autoantigens/immunology ; CD4-Positive T-Lymphocytes/immunology ; Clonal Deletion/immunology ; DNA-Binding Proteins/immunology ; Forkhead Transcription Factors ; Humans ; Mice ; Receptors, Antigen, T-Cell/immunology ; Self Tolerance/immunology
Chemical Substances	Autoantigens ; DNA-Binding Proteins ; FOXP3 protein, human ; Forkhead Transcription Factors ; Foxp3 protein, mouse ; Receptors, Antigen, T-Cell
Language	English
Publishing date	2005-04
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/ni1184
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Article ; Online: Two-step binding of transcription factors causes sequential chromatin structural changes at the activated IL-2 promoter.

Ishihara, Satoru / Schwartz, Ronald H

Journal of immunology (Baltimore, Md. : 1950)

2011 Volume 187, Issue 6, Page(s) 3292–3299

Abstract: Most gene promoters have multiple binding sequences for many transcription factors, but the contribution of each of these factors to chromatin remodeling is still unclear. Although we previously found a dynamic change in the arrangement of nucleosome ... ...

Abstract	Most gene promoters have multiple binding sequences for many transcription factors, but the contribution of each of these factors to chromatin remodeling is still unclear. Although we previously found a dynamic change in the arrangement of nucleosome arrays at the Il2 promoter during T cell activation, its timing preceded that of a decrease in nucleosome occupancy at the promoter. In this article, we show that the initial nucleosome rearrangement was temporally correlated with the binding of NFAT1 and AP-1 (Fos/Jun), whereas the second step occurred in parallel with the recruitment of other transcription factors and RNA polymerase II. Pharmacologic inhibitors for activation of NFAT1 or induction of Fos blocked the initial phase in the sequential changes. This step was not affected, however, by inhibition of c-Jun phosphorylation, which instead blocked the binding of the late transcription factors, the recruitment of CREB-binding protein, and the acetylation of histone H3 at lysine 27. Thus, the sequential recruitment of transcription factors appears to facilitate two separate steps in chromatin remodeling at the Il2 locus.
MeSH term(s)	Animals ; Blotting, Western ; CREB-Binding Protein/genetics ; CREB-Binding Protein/immunology ; CREB-Binding Protein/metabolism ; Chromatin/genetics ; Chromatin/immunology ; Chromatin/metabolism ; Chromatin Assembly and Disassembly/genetics ; Chromatin Assembly and Disassembly/immunology ; Chromatin Immunoprecipitation ; Female ; Interleukin-2/genetics ; Lymphocyte Activation/genetics ; Lymphocyte Activation/immunology ; Mice ; Mice, Transgenic ; NFATC Transcription Factors/genetics ; NFATC Transcription Factors/immunology ; NFATC Transcription Factors/metabolism ; Oligonucleotide Array Sequence Analysis ; Promoter Regions, Genetic/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction/genetics ; Signal Transduction/immunology ; T-Lymphocytes/immunology ; Transcription Factor AP-1/genetics ; Transcription Factor AP-1/immunology ; Transcription Factor AP-1/metabolism ; Transcription Factors/genetics ; Transcription Factors/immunology ; Transcription Factors/metabolism
Chemical Substances	Chromatin ; Interleukin-2 ; NFATC Transcription Factors ; Transcription Factor AP-1 ; Transcription Factors ; CREB-Binding Protein (EC 2.3.1.48)
Language	English
Publishing date	2011-08-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
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.1003173
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Article ; Online: Impairment of immunological synapse formation in adaptively tolerant T cells.

Choi, Seeyoung / Schwartz, Ronald H

Journal of immunology (Baltimore, Md. : 1950)

2011 Volume 187, Issue 2, Page(s) 805–816

Abstract: Adaptive tolerance is a hyporesponsive state in which lymphocyte Ag receptor signaling becomes desensitized after prolonged in vivo encounter with Ag. The molecular mechanisms underlying this hyporesponsive state in T cells are not fully understood, ... ...

Abstract	Adaptive tolerance is a hyporesponsive state in which lymphocyte Ag receptor signaling becomes desensitized after prolonged in vivo encounter with Ag. The molecular mechanisms underlying this hyporesponsive state in T cells are not fully understood, although a major signaling block has been shown to be present at the level of ZAP70 phosphorylation of linker for activation of T cells (LAT). In this study, we investigated the ability of adaptively tolerant mouse T cells to form conjugates with Ag-bearing APCs and to translocate signaling molecules into the interface between the T cells and APCs. Compared with naive or preactivated T cells, adaptively tolerant T cells showed no dramatic impairment in their formation of conjugates with APCs. In contrast, there was a large impairment in immunological synapse formation. Adaptively tolerant T cells were defective in their translocation of signaling molecules, such as ZAP70, LAT, and phospholipase C γ1, into the T cell-APC contact sites. Although Ag-induced activation of VAV1 was normal, VAV's recruitment into the synapse was also impaired. Interestingly, expressions of both IL-2-inducible T cell kinase and growth factor receptor-bound protein 2-related adaptor downstream of SHC were decreased by 60-80% in adaptively tolerant T cells. These decreases, in addition to the impairment in LAT phosphorylation by ZAP70, appear to be the major impediments to the phosphorylation of SLP76 (SRC homology 2 domain-containing leukocyte protein of 76 kDa) and the recruitment of VAV1, which are important for stable immunological synapse formation.
MeSH term(s)	Adaptive Immunity/genetics ; Adaptor Proteins, Signal Transducing/antagonists & inhibitors ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Antigen-Presenting Cells/immunology ; Antigen-Presenting Cells/metabolism ; Cell Line ; Clonal Anergy/genetics ; Down-Regulation/genetics ; Down-Regulation/immunology ; GRB2 Adaptor Protein/antagonists & inhibitors ; Immunological Synapses/genetics ; Membrane Proteins/antagonists & inhibitors ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred A ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Phosphorylation/immunology ; Protein Transport/immunology ; Protein-Tyrosine Kinases/antagonists & inhibitors ; Protein-Tyrosine Kinases/biosynthesis ; Proto-Oncogene Proteins c-vav ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; GRB2 Adaptor Protein ; GRB2 protein, human ; LAT protein, human ; Membrane Proteins ; Proto-Oncogene Proteins c-vav ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; emt protein-tyrosine kinase (EC 2.7.10.2)
Language	English
Publishing date	2011-06-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
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.1003314
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Article: T cell anergy.

Schwartz, Ronald H

Annual review of immunology

2003 Volume 21, Page(s) 305–334

Abstract: T cell anergy is a tolerance mechanism in which the lymphocyte is intrinsically functionally inactivated following an antigen encounter, but remains alive for an extended period of time in a hyporesponsive state. Models of T cell anergy affecting both ... ...

Abstract	T cell anergy is a tolerance mechanism in which the lymphocyte is intrinsically functionally inactivated following an antigen encounter, but remains alive for an extended period of time in a hyporesponsive state. Models of T cell anergy affecting both CD4(+) and CD8(+) cells fall into two broad categories. One, clonal anergy, is principally a growth arrest state, whereas the other, adaptive tolerance or in vivo anergy, represents a more generalized inhibition of proliferation and effector functions. The former arises from incomplete T cell activation, is mostly observed in previously activated T cells, is maintained by a block in the Ras/MAP kinase pathway, can be reversed by IL-2 or anti-OX40 signaling, and usually does not result in the inhibition of effector functions. The latter is most often initiated in naïve T cells in vivo by stimulation in an environment deficient in costimulation or high in coinhibition. Adaptive tolerance can be induced in the thymus or in the periphery. The cells proliferate and differentiate to varying degrees and then downregulate both functions in the face of persistent antigen. The state involves an early block in tyrosine kinase activation, which predominantly inhibits calcium mobilization, and an independent mechanism that blocks signaling through the IL-2 receptor. Adaptive tolerance reverses in the absence of antigen. Aspects of both of the anergic states are found in regulatory T cells, possibly preventing them from dominating initial immune responses to foreign antigens and shutting down such responses prematurely.
MeSH term(s)	Abatacept ; Adaptation, Physiological ; Adoptive Transfer ; Animals ; Antigen Presentation ; Antigens, CD ; Antigens, Differentiation/metabolism ; CD4-Positive T-Lymphocytes/cytology ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/cytology ; CD8-Positive T-Lymphocytes/immunology ; CTLA-4 Antigen ; Clonal Anergy ; Humans ; Immunoconjugates ; Intercellular Adhesion Molecule-1/metabolism ; Mice ; Models, Immunological ; T-Lymphocytes/cytology ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism
Chemical Substances	Antigens, CD ; Antigens, Differentiation ; CTLA-4 Antigen ; CTLA4 protein, human ; Ctla4 protein, mouse ; Immunoconjugates ; Intercellular Adhesion Molecule-1 (126547-89-5) ; Abatacept (7D0YB67S97)
Language	English
Publishing date	2003
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Review
ZDB-ID	604953-9
ISSN	1545-3278 ; 0732-0582
ISSN (online)	1545-3278
ISSN	0732-0582
DOI	10.1146/annurev.immunol.21.120601.141110
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Article ; Online: Induction of T cell anergy: integration of environmental cues and infectious tolerance.

Chappert, Pascal / Schwartz, Ronald H

Current opinion in immunology

2010 Volume 22, Issue 5, Page(s) 552–559

Abstract: Anergy is a state of long-term hyporesponsiveness in T cells that is characterized by an active repression of TCR signaling and IL-2 expression [1]. Several forms of anergy have been described and the past few years have brought to light an increasing ... ...

Abstract	Anergy is a state of long-term hyporesponsiveness in T cells that is characterized by an active repression of TCR signaling and IL-2 expression [1]. Several forms of anergy have been described and the past few years have brought to light an increasing number of 'anergic factors' involved in the induction and the active maintenance of the state in lymphocytes. The role of mTOR and other related metabolic sensors and regulators has recently emerged as of particular importance in broadening our view of anergy-inducing signals. We will discuss the role of these molecules in regulating the choice between anergy and activation, a decision faced by all T cells undergoing TCR stimulation. We will then explore the relationship between the induction of anergy and the induction of regulatory T cells as well as the potential crosstalk responsible for the phenomenon of infectious tolerance.
MeSH term(s)	Animals ; Clonal Anergy/immunology ; Cues ; Environmental Exposure ; Humans ; Infections/immunology ; Lymphocyte Activation/immunology ; Signal Transduction/immunology ; T-Lymphocytes/immunology
Language	English
Publishing date	2010-09-24
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	1035767-1
ISSN	1879-0372 ; 0952-7915
ISSN (online)	1879-0372
ISSN	0952-7915
DOI	10.1016/j.coi.2010.08.005
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Article ; Online: Pillars article: antigen presentation by chemically modified splenocytes induces antigen-specific T cell unresponsiveness in vitro and in vivo. J. Exp. Med. 1987. 165: 302-319.

Jenkins, Mark K / Schwartz, Ronald H

Journal of immunology (Baltimore, Md. : 1950)

2009 Volume 183, Issue 7, Page(s) 4150–4167

MeSH term(s)	Animals ; Antigen Presentation ; Cells, Cultured ; Cross-Linking Reagents/history ; Cross-Linking Reagents/metabolism ; Epitopes, T-Lymphocyte/history ; Epitopes, T-Lymphocyte/immunology ; Ethyldimethylaminopropyl Carbodiimide/history ; Ethyldimethylaminopropyl Carbodiimide/pharmacology ; History, 20th Century ; Immune Tolerance ; Mice ; Mice, Inbred A ; Mice, Inbred C57BL ; Spleen/drug effects ; Spleen/immunology ; T-Lymphocyte Subsets/immunology
Chemical Substances	Cross-Linking Reagents ; Epitopes, T-Lymphocyte ; Ethyldimethylaminopropyl Carbodiimide (RJ5OZG6I4A)
Language	English
Publishing date	2009-10-01
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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Article ; Online: Density dependent re-tuning of autoreactive T cells alleviates their pathogenicity in a lymphopenic environment.

Chuang, Eleanore / Augustine, Marilyn / Jung, Matthew / Schwartz, Ronald H / Singh, Nevil J

Immunology letters

2017 Volume 192, Page(s) 61–71

Abstract: Peripheral T cell tolerance is challenging to induce in partially lymphopenic hosts and this is relevant for clinical situations involving transplant tolerance. While the shortage of regulatory cells is thought to be one reason for this, T cell-intrinsic ...

Abstract	Peripheral T cell tolerance is challenging to induce in partially lymphopenic hosts and this is relevant for clinical situations involving transplant tolerance. While the shortage of regulatory cells is thought to be one reason for this, T cell-intrinsic tolerance processes such as anergy are also poorly triggered in such hosts. In order to understand the latter, we used a T cell deficient mouse model system where adoptively transferred autoreactive T cells are significantly tolerized in a cell intrinsic fashion, without differentiation to regulatory T cells. Intriguingly these T cells often retain sufficient effector functions to trigger autoimmune pathology. Here we find that the high population density of the autoreactive T cells that accumulated in such a host limits the progression of the cell-intrinsic tolerance process in T cells. Accordingly, reducing the cell density during a second transfer allowed T cells to further tune down their responsiveness to antigenic stimulation. The retuning of T cells was reflected by a loss of the T cell's abilities to proliferate, produces cytokines or help B cells. We further suggest, based on altering the levels of chronic antigen using miniosmotic pumps, that the effects of cell-density on T cell re-tuning may reflect the effective changes in the antigen dose perceived by individual T cells. This could proportionally elicit more negative feedback downstream of the TCR. Consistent with this, the retuned T cells showed signaling defects both proximal and distal to the TCR. Therefore, similar to the immunogenic activation of T cells, cell-intrinsic T cell tolerance may also involve a quantitative and progressive process of tuning down its antigen-responsiveness. The progress of such tuning seems to be stabilized at multiple intermediate stages by factors such as cell density, rather than just absolute antigen levels.
MeSH term(s)	Adoptive Transfer ; Animals ; Autoantigens/immunology ; Autoimmunity ; CD4-Positive T-Lymphocytes/immunology ; Cell Proliferation ; Cells, Cultured ; Cytokines/metabolism ; DNA-Binding Proteins/genetics ; Lymphocyte Activation ; Lymphopenia/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Peripheral Tolerance
Chemical Substances	Autoantigens ; Cytokines ; DNA-Binding Proteins ; Rag2 protein, mouse
Language	English
Publishing date	2017
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	445150-8
ISSN	1879-0542 ; 0165-2478
ISSN (online)	1879-0542
ISSN	0165-2478
DOI	10.1016/j.imlet.2017.10.005
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Article ; Online: Development and tolerization of hyperacute rejection in a transgenic mouse graft versus host model.

Oh, Soyoung / Schwartz, Ronald H / Singh, Nevil J

Transplantation

2012 Volume 94, Issue 3, Page(s) 234–240

Abstract: Background: The hyperacute rejection mediated by preexisting antibodies is a major impediment to the success of transplants across allogeneic and xenogeneic barriers. We report a new mouse model that allows us to not only monitor the sensitization of B ... ...

Abstract	Background: The hyperacute rejection mediated by preexisting antibodies is a major impediment to the success of transplants across allogeneic and xenogeneic barriers. We report a new mouse model that allows us to not only monitor the sensitization of B cells mediating the hyperacute response but also validate therapeutic strategies for tolerizing them. Model: The new model system uses 5C.C7,RAG2 T-cell receptor transgenic T cells and B10.S(9R),CD3[Latin Small Letter Open E] hosts for adoptive transfer experiments. Results and conclusions: In the allogeneic hosts, transgenic T cells expanded briefly before being chronically deleted. Once the deletion was initiated, a second graft of donor cells was used to assess a hyperacute response. The rapid rejection of the second cohort correlated with the appearance of donor-specific antibodies in the serum. Interestingly, chronically stimulated T cells were relatively resistant to hyperacute rejection, suggesting an explanation for the slower rejection kinetics of the first cohort even as the second cohort of identical donor cells was being hyperacutely rejected. Finally, we could tolerize the potential for a hyperacute response, by pretreating recipients with a single infusion of naive donor B cells before the first T-cell transfer. This treatment not only abrogated the development of a hyperacute response but also allowed the primary graft to survive in vivo for extended periods.
MeSH term(s)	Alleles ; Animals ; B-Lymphocytes/cytology ; Cell Separation ; Cohort Studies ; Crosses, Genetic ; Disease Models, Animal ; Flow Cytometry ; Graft Rejection/immunology ; Graft Survival ; Graft vs Host Reaction ; Mice ; Mice, Knockout ; Mice, Transgenic ; T-Lymphocytes/cytology
Language	English
Publishing date	2012-07-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	208424-7
ISSN	1534-6080 ; 0041-1337
ISSN (online)	1534-6080
ISSN	0041-1337
DOI	10.1097/TP.0b013e31825ccb91
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