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Article ; Online: How to Prevent yourself from Seeing Double.

Stadinski, Brian D / Huseby, Eric S

Cytometry. Part A : the journal of the International Society for Analytical Cytology

2020 Volume 97, Issue 11, Page(s) 1102–1104

MeSH term(s)	Biomarkers ; Monocytes ; T-Lymphocytes
Chemical Substances	Biomarkers
Language	English
Publishing date	2020-06-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	2099868-5
ISSN	1552-4930 ; 0196-4763 ; 1552-4922
ISSN (online)	1552-4930
ISSN	0196-4763 ; 1552-4922
DOI	10.1002/cyto.a.24045
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Article ; Online: I-A

Stadinski, Brian D / Cleveland, Sarah B / Brehm, Michael A / Greiner, Dale L / Huseby, Priya G / Huseby, Eric S

Nature immunology

2023 Volume 24, Issue 4, Page(s) 652–663

Abstract: Genetic susceptibility to type 1 diabetes is associated with homozygous expression of major histocompatibility complex class II alleles that carry specific beta chain polymorphisms. Why heterozygous expression of these major histocompatibility complex ... ...

Abstract	Genetic susceptibility to type 1 diabetes is associated with homozygous expression of major histocompatibility complex class II alleles that carry specific beta chain polymorphisms. Why heterozygous expression of these major histocompatibility complex class II alleles does not confer a similar predisposition is unresolved. Using a nonobese diabetic mouse model, here we show that heterozygous expression of the type 1 diabetes-protective allele I-A
MeSH term(s)	Mice ; Animals ; Diabetes Mellitus, Type 1 ; CD4-Positive T-Lymphocytes ; CD8-Positive T-Lymphocytes ; Histocompatibility Antigens Class II ; Insulin/metabolism ; Mice, Inbred NOD
Chemical Substances	Histocompatibility Antigens Class II ; Insulin
Language	English
Publishing date	2023-02-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/s41590-023-01441-0
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Article ; Online: Identifying environmental antigens that activate myelin-specific T cells.

Stadinski, Brian D / Huseby, Eric S

Trends in immunology

2014 Volume 35, Issue 6, Page(s) 231–232

Abstract: Human genetic and environmental factors underlie susceptibility to the T cell-mediated autoimmune disease, multiple sclerosis (MS). How the environment influences the pathogenesis of MS has been difficult to parse. A recent paper in Cell shows that ... ...

Abstract	Human genetic and environmental factors underlie susceptibility to the T cell-mediated autoimmune disease, multiple sclerosis (MS). How the environment influences the pathogenesis of MS has been difficult to parse. A recent paper in Cell shows that environmental antigens that activate myelin-specific T cells can be identified with unprecedented accuracy.
MeSH term(s)	Animals ; Humans ; Peptides/chemistry ; Receptors, Antigen, T-Cell/chemistry ; T-Lymphocytes/immunology
Chemical Substances	Peptides ; Receptors, Antigen, T-Cell
Language	English
Publishing date	2014-05-09
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	2036831-8
ISSN	1471-4981 ; 1471-4906
ISSN (online)	1471-4981
ISSN	1471-4906
DOI	10.1016/j.it.2014.04.004
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Article ; Online: CD4 Effector TCR Avidity for Peptide on APC Determines the Level of Memory Generated.

Jones, Michael C / Castonguay, Catherine / Nanaware, Padma P / Weaver, Grant C / Stadinski, Brian / Kugler-Umana, Olivia A / Huseby, Eric S / Stern, Lawrence J / McKinstry, Karl Kai / Strutt, Tara M / Devarajan, Priyadharshini / Swain, Susan L

Journal of immunology (Baltimore, Md. : 1950)

2023 Volume 210, Issue 12, Page(s) 1950–1961

Abstract: Initial TCR affinity for peptide Ag is known to impact the generation of memory; however, its contributions later, when effectors must again recognize Ag at 5-8 d postinfection to become memory, is unclear. We examined whether the effector TCR affinity ... ...

Abstract	Initial TCR affinity for peptide Ag is known to impact the generation of memory; however, its contributions later, when effectors must again recognize Ag at 5-8 d postinfection to become memory, is unclear. We examined whether the effector TCR affinity for peptide at this "effector checkpoint" dictates the extent of memory and degree of protection against rechallenge. We made an influenza A virus nucleoprotein (NP)-specific TCR transgenic mouse strain, FluNP, and generated NP-peptide variants that are presented by MHC class II to bind to the FluNP TCR over a broad range of avidity. To evaluate the impact of avidity in vivo, we primed naive donor FluNP in influenza A virus-infected host mice, purified donor effectors at the checkpoint, and cotransferred them with the range of peptides pulsed on activated APCs into second uninfected hosts. Higher-avidity peptides yielded higher numbers of FluNP memory cells in spleen and most dramatically in lung and draining lymph nodes and induced better protection against lethal influenza infection. Avidity determined memory cell number, not cytokine profile, and already impacted donor cell number within several days of transfer. We previously found that autocrine IL-2 production at the checkpoint prevents default effector apoptosis and supports memory formation. Here, we find that peptide avidity determines the level of IL-2 produced by these effectors and that IL-2Rα expression by the APCs enhances memory formation, suggesting that transpresentation of IL-2 by APCs further amplifies IL-2 availability. Secondary memory generation was also avidity dependent. We propose that this regulatory pathway selects CD4 effectors of highest affinity to progress to memory.
MeSH term(s)	Mice ; Animals ; CD4-Positive T-Lymphocytes/metabolism ; Interleukin-2/metabolism ; Peptides/metabolism ; Mice, Transgenic ; Receptors, Antigen, T-Cell/metabolism ; Immunologic Memory ; Mice, Inbred C57BL
Chemical Substances	Interleukin-2 ; Peptides ; Receptors, Antigen, T-Cell
Language	English
Publishing date	2023-10-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
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.2200337
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Article ; Online: A "hotspot" for autoimmune T cells in type 1 diabetes.

Stadinski, Brian D / Obst, Reinhard / Huseby, Eric S

The Journal of clinical investigation

2016 Volume 126, Issue 6, Page(s) 2040–2042

Abstract: The ability of a single T cell antigen receptor (TCR) to cross-react with multiple antigens allows the finite number of T cells within an organism to respond to the compendium of pathogen challenges faced during a lifetime. Effective immune surveillance, ...

Abstract	The ability of a single T cell antigen receptor (TCR) to cross-react with multiple antigens allows the finite number of T cells within an organism to respond to the compendium of pathogen challenges faced during a lifetime. Effective immune surveillance, however, comes at a price. TCR cross-reactivity can allow molecular mimics to spuriously activate autoimmune T cells; it also underlies T cell rejection of organ transplants and drives graft-versus-host disease. In this issue of the JCI, Cole and colleagues provide insight into how an insulin-reactive T cell cross-reacts with pathogen-derived antigens by focusing on a limited portion of the peptides to provide a hotspot for binding. These findings dovetail with recent studies of alloreactive and autoimmune TCRs and suggest that the biochemical principles that govern conventional protein-protein interactions may allow the specificity and cross-reactivity profiles of T cells to be predicted.
MeSH term(s)	Diabetes Mellitus, Type 1 ; Graft vs Host Disease/immunology ; Humans ; Peptides/chemistry ; Receptors, Antigen, T-Cell/chemistry ; T-Lymphocytes/cytology
Chemical Substances	Peptides ; Receptors, Antigen, T-Cell
Language	English
Publishing date	2016--01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI88165
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Article ; Online: Neonatal-derived IL-17 producing dermal γδ T cells are required to prevent spontaneous atopic dermatitis.

Spidale, Nicholas A / Malhotra, Nidhi / Frascoli, Michela / Sylvia, Katelyn / Miu, Bing / Freeman, Coral / Stadinski, Brian D / Huseby, Eric / Kang, Joonsoo

eLife

2020 Volume 9

Abstract: Atopic Dermatitis (AD) is a T cell-mediated chronic skin disease and is associated with altered skin barrier integrity. Infants with mutations in genes involved in tissue barrier fitness are predisposed towards inflammatory diseases, but most do not ... ...

Abstract	Atopic Dermatitis (AD) is a T cell-mediated chronic skin disease and is associated with altered skin barrier integrity. Infants with mutations in genes involved in tissue barrier fitness are predisposed towards inflammatory diseases, but most do not develop or sustain the diseases, suggesting that there exist regulatory immune mechanisms to prevent aberrant inflammation. The absence of one single murine dermal cell type, the innate neonatal-derived IL-17 producing γδ T (Tγδ17) cells, from birth resulted in spontaneous, highly penetrant AD with many of the major hallmarks of human AD. In Tγδ17 cell-deficient mice, basal keratinocyte transcriptome was altered months in advance of AD induction. Tγδ17 cells respond to skin commensal bacteria and the fulminant disease in their absence was driven by skin commensal bacteria dysbiosis. AD in this model was characterized by highly expanded dermal αβ T clonotypes that produce the type three cytokines, IL-17 and IL-22. These results demonstrate that neonatal Tγδ17 cells are innate skin regulatory T cells that are critical for skin homeostasis, and that IL-17 has dual homeostatic and inflammatory function in the skin.
MeSH term(s)	Animals ; Animals, Newborn ; Autoantigens/genetics ; Cell Differentiation ; Dermatitis, Atopic/genetics ; Dermatitis, Atopic/immunology ; Dermatitis, Atopic/prevention & control ; Disease Models, Animal ; Gene Expression ; Interleukin-17/biosynthesis ; Interleukins/biosynthesis ; Keratinocytes/cytology ; Keratinocytes/metabolism ; Lymphocyte Activation ; Mice ; Mice, Knockout ; Receptors, Antigen, T-Cell, gamma-delta/immunology ; Receptors, Antigen, T-Cell, gamma-delta/metabolism ; Skin/metabolism ; Skin/microbiology ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; Interleukin-22
Chemical Substances	Autoantigens ; Il17a protein, mouse ; Interleukin-17 ; Interleukins ; Receptors, Antigen, T-Cell, gamma-delta ; Sox13 protein, mouse
Language	English
Publishing date	2020-02-17
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.51188
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Article ; Online: A temporal thymic selection switch and ligand binding kinetics constrain neonatal Foxp3

Stadinski, Brian D / Blevins, Sydney J / Spidale, Nicholas A / Duke, Brian R / Huseby, Priya G / Stern, Lawrence J / Huseby, Eric S

Nature immunology

2019 Volume 20, Issue 8, Page(s) 1046–1058

Abstract: The neonatal thymus generates ... ...

Abstract	The neonatal thymus generates Foxp3
MeSH term(s)	Animals ; Autoantigens/immunology ; Autoimmunity/immunology ; Cell Differentiation/immunology ; Cell Line ; Female ; Forkhead Transcription Factors/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Protein-Arginine Deiminases/metabolism ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; Self Tolerance/immunology ; T-Lymphocytes, Regulatory/cytology ; T-Lymphocytes, Regulatory/immunology ; Thymus Gland/cytology
Chemical Substances	Autoantigens ; Forkhead Transcription Factors ; Foxp3 protein, mouse ; Receptors, Antigen, T-Cell, alpha-beta ; Padi4 protein, mouse (EC 3.5.3.15) ; Protein-Arginine Deiminases (EC 3.5.3.15)
Language	English
Publishing date	2019-06-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/s41590-019-0414-1
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Article ; Online: Molecular targeting of islet autoantigens.

Stadinski, Brian / Kappler, John / Eisenbarth, George S

Immunity

2010 Volume 32, Issue 4, Page(s) 446–456

Abstract: Type 1 diabetes of man and animal models results from immune-mediated specific beta cell destruction. Multiple islet antigens are targets of autoimmunity and most of these are not beta cell specific. Immune responses to insulin appear to be essential for ...

Abstract	Type 1 diabetes of man and animal models results from immune-mediated specific beta cell destruction. Multiple islet antigens are targets of autoimmunity and most of these are not beta cell specific. Immune responses to insulin appear to be essential for the development of diabetes of the NOD mouse. In this review, we will emphasize the unusual manner in which selected autoantigenic peptides (particularly the recently discovered target of BDC2.5 T cells [chromagranin A]) are presented and recognized by autoreactive CD4(+) T cell receptors. We hypothesize that "unusual" structural interactions of specific trimolecular complexes (MHC class II, peptide, and T cell receptors) are fundamental to the escape from the thymus of autoreactive T cells able to cause type 1 diabetes.
MeSH term(s)	Animals ; Autoantigens/immunology ; Diabetes Mellitus, Type 1/immunology ; Histocompatibility Antigens Class II/immunology ; Humans ; Islets of Langerhans/immunology ; Receptors, Antigen, T-Cell/immunology ; T-Lymphocytes/immunology
Chemical Substances	Autoantigens ; Histocompatibility Antigens Class II ; Receptors, Antigen, T-Cell
Language	English
Publishing date	2010-04-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2010.04.008
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Zs.A 4227: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Response to Garcia et al.

Huseby, Eric S / Stadinski, Brian D / Trenh, Peter / Stern, Lawrence J

Immunity

2012 Volume 36, Issue 6, Page(s) 889–890

MeSH term(s)	Animals ; Histocompatibility Antigens/chemistry ; Histocompatibility Antigens/genetics ; Histocompatibility Antigens/immunology ; Receptors, Antigen, T-Cell, alpha-beta
Chemical Substances	Histocompatibility Antigens ; Receptors, Antigen, T-Cell, alpha-beta
Language	English
Publishing date	2012-06-14
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2012.05.019
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Article ; Online: Pathogenic CD8 T cells in multiple sclerosis and its experimental models.

Huseby, Eric S / Huseby, Priya G / Shah, Shivanee / Smith, Rebecca / Stadinski, Brian D

Frontiers in immunology

2012 Volume 3, Page(s) 64

Abstract: A growing body of evidence suggests that autoreactive CD8 T cells contribute to the disease process in multiple sclerosis (MS). Lymphocytes in MS plaques are biased toward the CD8 lineage, and MS patients harbor CD8 T cells specific for multiple central ... ...

Abstract	A growing body of evidence suggests that autoreactive CD8 T cells contribute to the disease process in multiple sclerosis (MS). Lymphocytes in MS plaques are biased toward the CD8 lineage, and MS patients harbor CD8 T cells specific for multiple central nervous system (CNS) antigens. Currently, there are relatively few experimental model systems available to study these pathogenic CD8 T cells in vivo. However, the few studies that have been done characterizing the mechanisms used by CD8 T cells to induce CNS autoimmunity indicate that several of the paradigms of how CD4 T cells mediate CNS autoimmunity do not hold true for CD8 T cells or for patients with MS. Thus, myelin-specific CD4 T cells are likely to be one of several important mechanisms that drive CNS disease in MS patients. The focus of this review is to highlight the current models of pathogenic CNS-reactive CD8 T cells and the molecular mechanisms these lymphocytes use when causing CNS inflammation and damage. Understanding how CNS-reactive CD8 T cells escape tolerance induction and induce CNS autoimmunity is critical to our ability to propose and test new therapies for MS.
Language	English
Publishing date	2012-03-29
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2012.00064
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