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Article ; Online: T cells in the control of organ-specific autoimmunity.

Bluestone, Jeffrey A / Bour-Jordan, Hélène / Cheng, Mickie / Anderson, Mark

2015 Volume 125, Issue 6, Page(s) 2250–2260

Abstract: Immune tolerance is critical to the avoidance of unwarranted immune responses against self antigens. Multiple, non-redundant checkpoints are in place to prevent such potentially deleterious autoimmune responses while preserving immunity integral to the ... ...

Abstract	Immune tolerance is critical to the avoidance of unwarranted immune responses against self antigens. Multiple, non-redundant checkpoints are in place to prevent such potentially deleterious autoimmune responses while preserving immunity integral to the fight against foreign pathogens. Nevertheless, a large and growing segment of the population is developing autoimmune diseases. Deciphering cellular and molecular pathways of immune tolerance is an important goal, with the expectation that understanding these pathways will lead to new clinical advances in the treatment of these devastating diseases. The vast majority of autoimmune diseases develop as a consequence of complex mechanisms that depend on genetic, epigenetic, molecular, cellular, and environmental elements and result in alterations in many different checkpoints of tolerance and ultimately in the breakdown of immune tolerance. The manifestations of this breakdown are harmful inflammatory responses in peripheral tissues driven by innate immunity and self antigen-specific pathogenic T and B cells. T cells play a central role in the regulation and initiation of these responses. In this Review we summarize our current understanding of the mechanisms involved in these fundamental checkpoints, the pathways that are defective in autoimmune diseases, and the therapeutic strategies being developed with the goal of restoring immune tolerance.
MeSH term(s)	Animals ; Autoimmune Diseases/immunology ; Autoimmune Diseases/pathology ; Autoimmune Diseases/therapy ; Autoimmunity ; B-Lymphocytes/immunology ; B-Lymphocytes/pathology ; Humans ; Immune Tolerance ; Immunity, Innate ; Organ Specificity/immunology ; T-Lymphocytes/immunology ; T-Lymphocytes/pathology
Language	English
Publishing date	2015-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI78089
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Article ; Online: Breakdown in peripheral tolerance in type 1 diabetes in mice and humans.

Jeker, Lukas T / Bour-Jordan, Hélène / Bluestone, Jeffrey A

Cold Spring Harbor perspectives in medicine

2012 Volume 2, Issue 3, Page(s) a007807

Abstract: Type 1 Diabetes (T1D), also called juvenile diabetes because of its classically early onset, is considered an autoimmune disease targeting the insulin-producing β cells in the pancreatic islets of Langerhans. T1D reflects a loss of tolerance to tissue ... ...

Abstract	Type 1 Diabetes (T1D), also called juvenile diabetes because of its classically early onset, is considered an autoimmune disease targeting the insulin-producing β cells in the pancreatic islets of Langerhans. T1D reflects a loss of tolerance to tissue self-antigens caused by defects in both central tolerance, which aims at eliminating potentially autoreactive lymphocytes developing in the thymus, and peripheral tolerance, which normally controls autoreactive T cells that escaped the thymus. Like in other autoimmune diseases, the mechanisms leading to T1D are multifactorial and depend on a complex combination of genetic, epigenetic, molecular, and cellular elements that result in the breakdown of peripheral tolerance. In this article, we discuss the contribution of these factors in the development of the autoimmune response targeting pancreatic islets in T1D and the therapeutic strategies currently being explored to correct these defects.
MeSH term(s)	Animals ; Autoantigens/immunology ; Autoimmunity/immunology ; CTLA-4 Antigen/immunology ; Diabetes Mellitus, Type 1/immunology ; Disease Progression ; Genome-Wide Association Study ; Humans ; Interleukin-2/immunology ; Islets of Langerhans/physiology ; Mice ; Mice, Inbred NOD ; Peripheral Tolerance/immunology ; T-Lymphocytes, Regulatory/immunology
Chemical Substances	Autoantigens ; CTLA-4 Antigen ; Interleukin-2
Language	English
Publishing date	2012-03-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ISSN	2157-1422
ISSN (online)	2157-1422
DOI	10.1101/cshperspect.a007807
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Article ; Online: Current and future immunomodulation strategies to restore tolerance in autoimmune diseases.

Bluestone, Jeffrey A / Bour-Jordan, Hélène

Cold Spring Harbor perspectives in biology

2012 Volume 4, Issue 11

Abstract: Autoimmune diseases reflect a breakdown in self-tolerance that results from defects in thymic deletion of potentially autoreactive T cells (central tolerance) and in T-cell intrinsic and extrinsic mechanisms that normally control potentially autoreactive ...

Abstract	Autoimmune diseases reflect a breakdown in self-tolerance that results from defects in thymic deletion of potentially autoreactive T cells (central tolerance) and in T-cell intrinsic and extrinsic mechanisms that normally control potentially autoreactive T cells in the periphery (peripheral tolerance). The mechanisms leading to autoimmune diseases are multifactorial and depend on a complex combination of genetic, epigenetic, molecular, and cellular elements that result in pathogenic inflammatory responses in peripheral tissues driven by self-antigen-specific T cells. In this article, we describe the different checkpoints of tolerance that are defective in autoimmune diseases as well as specific events in the autoimmune response which represent therapeutic opportunities to restore long-term tolerance in autoimmune diseases. We present evidence for the role of different pathways in animal models and the therapeutic strategies targeting these pathways in clinical trials in autoimmune diseases.
MeSH term(s)	Animals ; Autoimmune Diseases/immunology ; Autoimmune Diseases/physiopathology ; Autoimmune Diseases/therapy ; Humans ; Immune Tolerance ; Immunotherapy/methods ; Peripheral Tolerance/immunology ; T-Lymphocytes/immunology
Language	English
Publishing date	2012-11-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ISSN	1943-0264
ISSN (online)	1943-0264
DOI	10.1101/cshperspect.a007542
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Article ; Online: How suppressor cells led to anergy, costimulation, and beyond.

Bour-Jordan, Hélène / Bluestone, Jeffery A

Journal of immunology (Baltimore, Md. : 1950)

2009 Volume 183, Issue 7, Page(s) 4147–4149

MeSH term(s)	Animals ; Antigen Presentation ; Clonal Anergy/immunology ; Epitopes, T-Lymphocyte/history ; Epitopes, T-Lymphocyte/physiology ; History, 20th Century ; Immune Tolerance ; Lymphocyte Activation/immunology ; Mice ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism
Chemical Substances	Epitopes, T-Lymphocyte
Language	English
Publishing date	2009-10-01
Publishing country	United States
Document type	Comment ; 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
DOI	10.4049/jimmunol.0990078
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Article ; Online: Regulating the regulators: costimulatory signals control the homeostasis and function of regulatory T cells.

Bour-Jordan, Hélène / Bluestone, Jeffrey A

Immunological reviews

2009 Volume 229, Issue 1, Page(s) 41–66

Abstract: Summary: Costimulation is a concept that goes back to the early 1980s when Lafferty and others hypothesized that cell surface and soluble molecules must exist that are essential for initiating immune responses subsequent to antigen exposure. The ... ...

Abstract	Summary: Costimulation is a concept that goes back to the early 1980s when Lafferty and others hypothesized that cell surface and soluble molecules must exist that are essential for initiating immune responses subsequent to antigen exposure. The explosion in this field of research ensued as over a dozen molecules have been identified to function as second signals following T-cell receptor engagement. By 1994, it seemed clear that the most prominent costimulatory pathway CD28 and functionally related costimulatory molecules, such as CD154, were the major drivers of a positive immune response. Then the immunology world turned upside down. CD28 knockout mice, which were, in most cases, immunodeficient, led to increased autoimmunity when bred into the non-obese diabetic background. Another CD28 family member, cytotoxic T-lymphocyte-associated protein 4, which was presumed to be a costimulatory molecule on activated T cells, turned out to be critical in downregulating immunity. These results, coupled with the vast suppressor cell literature which had been largely rebuked, suggested that the immune system was not poised for response but controlled in such a way that regulation was dominant. Over the last decade, we have learned that these costimulatory molecules play a key role in the now classical CD4(+)CD25(+)Foxp3(+) regulatory T cells (Tregs) that provide critical control of unwanted autoimmune responses. In this review, we discuss the connections between costimulation and Tregs that have changed the costimulation paradigm.
MeSH term(s)	Animals ; Antigens, CD/immunology ; Antigens, CD/metabolism ; B7-1 Antigen/immunology ; B7-1 Antigen/metabolism ; CD28 Antigens/immunology ; CD28 Antigens/metabolism ; CTLA-4 Antigen ; Forkhead Transcription Factors/immunology ; Forkhead Transcription Factors/metabolism ; Humans ; Lymphocyte Activation/immunology ; Mice ; Signal Transduction/immunology ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism ; Thymus Gland/immunology ; Thymus Gland/metabolism
Chemical Substances	Antigens, CD ; B7-1 Antigen ; CD28 Antigens ; CTLA-4 Antigen ; CTLA4 protein, human ; Ctla4 protein, mouse ; Forkhead Transcription Factors
Language	English
Publishing date	2009-05-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	391796-4
ISSN	1600-065X ; 0105-2896
ISSN (online)	1600-065X
ISSN	0105-2896
DOI	10.1111/j.1600-065X.2009.00775.x
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Article: Regulating the regulators: costimulatory signals control the homeostasis and function of regulatory T cells

Bour-Jordan, Hélène / Bluestone, Jeffrey A

Immunological reviews. 2009 May, v. 229, no. 1

2009

Abstract: Costimulation is a concept that goes back to the early 1980s when Lafferty and others hypothesized that cell surface and soluble molecules must exist that are essential for initiating immune responses subsequent to antigen exposure. The explosion in this ...

Abstract	Costimulation is a concept that goes back to the early 1980s when Lafferty and others hypothesized that cell surface and soluble molecules must exist that are essential for initiating immune responses subsequent to antigen exposure. The explosion in this field of research ensued as over a dozen molecules have been identified to function as second signals following T-cell receptor engagement. By 1994, it seemed clear that the most prominent costimulatory pathway CD28 and functionally related costimulatory molecules, such as CD154, were the major drivers of a positive immune response. Then the immunology world turned upside down. CD28 knockout mice, which were, in most cases, immunodeficient, led to increased autoimmunity when bred into the non-obese diabetic background. Another CD28 family member, cytotoxic T-lymphocyte-associated protein 4, which was presumed to be a costimulatory molecule on activated T cells, turned out to be critical in downregulating immunity. These results, coupled with the vast suppressor cell literature which had been largely rebuked, suggested that the immune system was not poised for response but controlled in such a way that regulation was dominant. Over the last decade, we have learned that these costimulatory molecules play a key role in the now classical CD4⁺CD25⁺Foxp3⁺ regulatory T cells (Tregs) that provide critical control of unwanted autoimmune responses. In this review, we discuss the connections between costimulation and Tregs that have changed the costimulation paradigm.
Language	English
Dates of publication	2009-05
Size	p. 41-66.
Publisher	Blackwell Publishing Ltd
Publishing place	Oxford, UK
Document type	Article
ZDB-ID	391796-4
ISSN	1600-065X ; 0105-2896
ISSN (online)	1600-065X
ISSN	0105-2896
DOI	10.1111/j.1600-065X.2009.00775.x
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Article: B cell depletion: a novel therapy for autoimmune diabetes?

Bour-Jordan, Hélène / Bluestone, Jeffrey A

The Journal of clinical investigation

2007 Volume 117, Issue 12, Page(s) 3642–3645

Abstract: Autoimmune diabetes is believed to be mediated primarily by T cells. However, B cells have been implicated in the pathogenesis of the disease in NOD mice. Although preclinical studies have been limited by the absence of anti-CD20 reagents that can induce ...

Abstract	Autoimmune diabetes is believed to be mediated primarily by T cells. However, B cells have been implicated in the pathogenesis of the disease in NOD mice. Although preclinical studies have been limited by the absence of anti-CD20 reagents that can induce B cell depletion in mice, a clinical trial using the B cell-depleting anti-CD20 monoclonal antibody rituximab (Rituxan) is underway in type 1 diabetes patients. In this issue of the JCI, Hu et al. describe the generation of transgenic NOD mice that express human CD20 on B cells (see the related article beginning on page 3857). They show that anti-CD20 therapy induces B cell depletion in these mice and offers some level of protection against diabetes. Although many questions remain unanswered, this mouse model represents the first opportunity to evaluate the potential value of rituximab as a novel therapy for autoimmune diabetes.
MeSH term(s)	Animals ; Antibodies, Monoclonal/pharmacology ; Antibodies, Monoclonal/therapeutic use ; Antigen Presentation/drug effects ; Antigens, CD20/genetics ; Antigens, CD20/immunology ; Autoantibodies/immunology ; B-Lymphocytes/immunology ; B-Lymphocytes/pathology ; Cytokines/immunology ; Diabetes Mellitus, Type 1/drug therapy ; Diabetes Mellitus, Type 1/genetics ; Diabetes Mellitus, Type 1/immunology ; Diabetes Mellitus, Type 1/pathology ; Humans ; Hyperglycemia/drug therapy ; Hyperglycemia/genetics ; Hyperglycemia/immunology ; Lymphocyte Depletion ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/pathology
Chemical Substances	Antibodies, Monoclonal ; Antigens, CD20 ; Autoantibodies ; Cytokines
Language	English
Publishing date	2007-10-11
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI34236
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Article: Sensory neurons link the nervous system and autoimmune diabetes.

Bour-Jordan, Helene / Bluestone, Jeffrey A

Cell

2006 Volume 127, Issue 6, Page(s) 1097–1099

Abstract: The initial factors that trigger the autoimmune response against pancreatic islets in the nonobese diabetic (NOD) mouse are still unknown. In this issue of Cell, propose that a defect in a subset of sensory neurons innervating the pancreas plays a major ... ...

Abstract	The initial factors that trigger the autoimmune response against pancreatic islets in the nonobese diabetic (NOD) mouse are still unknown. In this issue of Cell, propose that a defect in a subset of sensory neurons innervating the pancreas plays a major role in initiating the chain of events that will lead to local inflammation, islet destruction, and autoimmune diabetes.
MeSH term(s)	Animals ; Autoimmunity ; Diabetes Mellitus, Type 1/immunology ; Diabetes Mellitus, Type 1/physiopathology ; Humans ; Inflammation/physiopathology ; Islets of Langerhans/immunology ; Islets of Langerhans/innervation ; Mice ; Mice, Inbred NOD ; Neurons, Afferent/physiology ; Neurosecretory Systems/physiology ; TRPV Cation Channels/genetics
Chemical Substances	TRPV Cation Channels ; TRPV1 protein, mouse
Language	English
Publishing date	2006-12-15
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2006.11.030
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Article: Distinct effector mechanisms in the development of autoimmune neuropathy versus diabetes in nonobese diabetic mice.

Bour-Jordan, Hélène / Thompson, Heather L / Bluestone, Jeffrey A

Journal of immunology (Baltimore, Md. : 1950)

2005 Volume 175, Issue 9, Page(s) 5649–5655

Abstract: NOD mice deficient for the costimulatory molecule B7-2 (NOD-B7-2KO mice) are protected from autoimmune diabetes but develop a spontaneous autoimmune peripheral neuropathy that resembles human diseases Guillain-Barre syndrome and chronic inflammatory ... ...

Abstract	NOD mice deficient for the costimulatory molecule B7-2 (NOD-B7-2KO mice) are protected from autoimmune diabetes but develop a spontaneous autoimmune peripheral neuropathy that resembles human diseases Guillain-Barre syndrome and chronic inflammatory demyelinating polyradiculoneuropathy. Similar observations have now been made in conventional NOD mice. We have shown previously that this disease was mediated by autoreactive T cells inducing demyelination in the peripheral nervous system. In this study, we analyzed the molecular pathways involved in the disease. Our data showed that neuropathy developed in the absence of perforin or fas, suggesting that classic cytotoxicity pathways were dispensable for nerve damage in NOD-B7-2KO mice. In contrast, IFN-gamma played an obligatory role in the development of neuropathy as demonstrated by the complete protection from disease and infiltration in the nerves in NOD-B7-2KO mice deficient for IFN-gamma. This result was consistent with the inflammatory phenotype of T cells infiltrating the peripheral nerves. Importantly, the relative role of perforin, fas, and IFN-gamma appears completely different in autoimmune diabetes vs neuropathy. Thus, there are sharp contrasts in the pathogenesis of autoimmune diseases targeting different tissues in the same NOD background.
MeSH term(s)	Animals ; Autoimmune Diseases/etiology ; B7-2 Antigen/physiology ; Diabetes Mellitus, Type 1/etiology ; Interferon-gamma/biosynthesis ; Membrane Glycoproteins/physiology ; Mice ; Mice, Inbred NOD ; Mice, Knockout ; Perforin ; Peripheral Nervous System Diseases/etiology ; Pore Forming Cytotoxic Proteins ; Th1 Cells/physiology
Chemical Substances	B7-2 Antigen ; Membrane Glycoproteins ; Pore Forming Cytotoxic Proteins ; Perforin (126465-35-8) ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2005-09-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
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.175.9.5649
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Article ; Online: Distinct genetic control of autoimmune neuropathy and diabetes in the non-obese diabetic background.

Bour-Jordan, Hélène / Thompson, Heather L / Giampaolo, Jennifer R / Davini, Dan / Rosenthal, Wendy / Bluestone, Jeffrey A

Journal of autoimmunity

2013 Volume 45, Page(s) 58–67

Abstract: The non-obese diabetic (NOD) mouse is susceptible to the development of autoimmune diabetes but also multiple other autoimmune diseases. Over twenty susceptibility loci linked to diabetes have been identified in NOD mice and progress has been made in the ...

Abstract	The non-obese diabetic (NOD) mouse is susceptible to the development of autoimmune diabetes but also multiple other autoimmune diseases. Over twenty susceptibility loci linked to diabetes have been identified in NOD mice and progress has been made in the definition of candidate genes at many of these loci (termed Idd for insulin-dependent diabetes). The susceptibility to multiple autoimmune diseases in the NOD background is a unique opportunity to examine susceptibility genes that confer a general propensity for autoimmunity versus susceptibility genes that control individual autoimmune diseases. We previously showed that NOD mice deficient for the costimulatory molecule B7-2 (NOD-B7-2KO mice) were protected from diabetes but spontaneously developed an autoimmune peripheral neuropathy. Here, we took advantage of multiple NOD mouse strains congenic for Idd loci to test the role of these Idd loci the development of neuropathy and determine if B6 alleles at Idd loci that are protective for diabetes will also be for neuropathy. Thus, we generated NOD-B7-2KO strains congenic at Idd loci and examined the development of neuritis and clinical neuropathy. We found that the NOD-H-2(g7) MHC region is necessary for development of neuropathy in NOD-B7-2KO mice. In contrast, other Idd loci that significantly protect from diabetes did not affect neuropathy when considered individually. However, we found potent genetic interactions of some Idd loci that provided almost complete protection from neuritis and clinical neuropathy. In addition, defective immunoregulation by Tregs could supersede protection by some, but not other, Idd loci in a tissue-specific manner in a model where neuropathy and diabetes occurred concomitantly. Thus, our study helps identify Idd loci that control tissue-specific disease or confer general susceptibility to autoimmunity, and brings insight to the Treg-dependence of autoimmune processes influenced by given Idd region in the NOD background.
MeSH term(s)	Alleles ; Animals ; B7-2 Antigen/genetics ; Cells, Cultured ; Diabetes Mellitus, Type 1/complications ; Diabetes Mellitus, Type 1/genetics ; Diabetes Mellitus, Type 1/immunology ; Female ; Genetic Loci/genetics ; Genetic Predisposition to Disease/genetics ; Guillain-Barre Syndrome/complications ; Guillain-Barre Syndrome/genetics ; Guillain-Barre Syndrome/immunology ; Histocompatibility Antigens Class II/genetics ; Interferon-gamma/metabolism ; Male ; Mice ; Mice, Congenic ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, Knockout ; Organ Specificity ; Sex Factors ; T-Lymphocytes, Regulatory/immunology
Chemical Substances	B7-2 Antigen ; Histocompatibility Antigens Class II ; I-A g7 antigen ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2013-07-12
Publishing country	England
Document type	Journal Article
ZDB-ID	639452-8
ISSN	1095-9157 ; 0896-8411
ISSN (online)	1095-9157
ISSN	0896-8411
DOI	10.1016/j.jaut.2013.06.005
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