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Article ; Online: Roles of Adenosine Receptor (subtypes A

Adebiyi, Olamide E / Bynoe, Margaret S

2023 Volume 60, Issue 10, Page(s) 5878–5890

Abstract: Hippocampal demyelination in multiple sclerosis (MS) has been linked with cognitive deficits, however, patients could benefit from treatment that induces oligodendroglial cell function and promotes remyelination. We investigated the role of ... ...

Abstract	Hippocampal demyelination in multiple sclerosis (MS) has been linked with cognitive deficits, however, patients could benefit from treatment that induces oligodendroglial cell function and promotes remyelination. We investigated the role of A
MeSH term(s)	Mice ; Animals ; Cuprizone/toxicity ; Demyelinating Diseases/pathology ; Disease Models, Animal ; Mice, Inbred C57BL ; Myelin Sheath/metabolism ; Oligodendroglia/metabolism ; Multiple Sclerosis/pathology ; Hippocampus/metabolism ; Receptors, Purinergic P1/metabolism
Chemical Substances	Cuprizone (5N16U7E0AO) ; Receptors, Purinergic P1
Language	English
Publishing date	2023-06-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-023-03440-6
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Article ; Online: A2A adenosine receptor modulates drug efflux transporter P-glycoprotein at the blood-brain barrier.

Kim, Do-Geun / Bynoe, Margaret S

The Journal of clinical investigation

2016 Volume 126, Issue 5, Page(s) 1717–1733

Abstract: The blood-brain barrier (BBB) protects the brain from toxic substances within the peripheral circulation. It maintains brain homeostasis and is a hurdle for drug delivery to the CNS to treat neurodegenerative diseases, including Alzheimer's disease and ... ...

Abstract	The blood-brain barrier (BBB) protects the brain from toxic substances within the peripheral circulation. It maintains brain homeostasis and is a hurdle for drug delivery to the CNS to treat neurodegenerative diseases, including Alzheimer's disease and brain tumors. The drug efflux transporter P-glycoprotein (P-gp) is highly expressed on brain endothelial cells and blocks the entry of most drugs delivered to the brain. Here, we show that activation of the A2A adenosine receptor (AR) with an FDA-approved A2A AR agonist (Lexiscan) rapidly and potently decreased P-gp expression and function in a time-dependent and reversible manner. We demonstrate that downmodulation of P-gp expression and function coincided with chemotherapeutic drug accumulation in brains of WT mice and in primary mouse and human brain endothelial cells, which serve as in vitro BBB models. Lexiscan also potently downregulated the expression of BCRP1, an efflux transporter that is highly expressed in the CNS vasculature and other tissues. Finally, we determined that multiple pathways, including MMP9 cleavage and ubiquitinylation, mediated P-gp downmodulation. Based on these data, we propose that A2A AR activation on BBB endothelial cells offers a therapeutic window that can be fine-tuned for drug delivery to the brain and has potential as a CNS drug-delivery technology.
MeSH term(s)	ATP Binding Cassette Transporter, Subfamily B/biosynthesis ; ATP Binding Cassette Transporter, Subfamily B/genetics ; ATP Binding Cassette Transporter, Subfamily G, Member 2/biosynthesis ; ATP Binding Cassette Transporter, Subfamily G, Member 2/blood ; ATP Binding Cassette Transporter, Subfamily G, Member 2/genetics ; Adenosine A2 Receptor Agonists/pharmacology ; Animals ; Blood-Brain Barrier/metabolism ; Cell Line ; Endothelial Cells/metabolism ; Gene Expression Regulation ; Humans ; Matrix Metalloproteinase 9/genetics ; Matrix Metalloproteinase 9/metabolism ; Mice ; Neoplasm Proteins/blood ; Neoplasm Proteins/genetics ; Proteolysis/drug effects ; Purines/pharmacology ; Pyrazoles/pharmacology ; Receptor, Adenosine A2A/genetics ; Receptor, Adenosine A2A/metabolism ; Ubiquitination/drug effects ; Ubiquitination/genetics
Chemical Substances	ABCB1 protein, human ; ABCG2 protein, human ; ATP Binding Cassette Transporter, Subfamily B ; ATP Binding Cassette Transporter, Subfamily G, Member 2 ; Abcg2 protein, mouse ; Adenosine A2 Receptor Agonists ; Neoplasm Proteins ; Purines ; Pyrazoles ; Receptor, Adenosine A2A ; regadenoson (2XLN4Y044H) ; MMP9 protein, human (EC 3.4.24.35) ; Matrix Metalloproteinase 9 (EC 3.4.24.35) ; Mmp9 protein, mouse (EC 3.4.24.35)
Language	English
Publishing date	2016-04-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI76207
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Article ; Online: A2A Adenosine Receptor Regulates the Human Blood-Brain Barrier Permeability.

Kim, Do-Geun / Bynoe, Margaret S

Molecular neurobiology

2014 Volume 52, Issue 1, Page(s) 664–678

Abstract: The blood-brain barrier (BBB) symbolically represents the gateway to the central nervous system. It is a single layer of specialized endothelial cells that coats the central nervous system (CNS) vasculature and physically separates the brain environment ... ...

Abstract	The blood-brain barrier (BBB) symbolically represents the gateway to the central nervous system. It is a single layer of specialized endothelial cells that coats the central nervous system (CNS) vasculature and physically separates the brain environment from the blood constituents to maintain the homeostasis of the CNS. However, this protective measure is a hindrance to the delivery of therapeutics to treat neurological diseases. Here, we show that activation of A2A adenosine receptor (AR) with an FDA-approved agonist potently permeabilizes an in vitro primary human BBB (hBBB) to the passage of chemotherapeutic drugs and T cells. T cell migration under AR signaling occurs primarily by paracellular transendothelial route. Permeabilization of the hBBB is rapid, time-dependent, and reversible and is mediated by morphological changes in actin-cytoskeletal reorganization induced by RhoA signaling and a potent downregulation of claudin-5 and VE-cadherin. Moreover, the kinetics of BBB permeability in mice closely overlaps with the permeability kinetics of the hBBB. These data suggest that activation of A2A AR is an endogenous mechanism that may be used for CNS drug delivery in human.
MeSH term(s)	Adenosine A2 Receptor Agonists/pharmacology ; Adherens Junctions/drug effects ; Adherens Junctions/metabolism ; Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Blood-Brain Barrier/metabolism ; Cell Death/drug effects ; Cell Line ; Cell Membrane Permeability/drug effects ; Cell Movement/drug effects ; Deoxycytidine/analogs & derivatives ; Deoxycytidine/pharmacology ; Down-Regulation/drug effects ; Electric Impedance ; Endothelial Cells/cytology ; Endothelial Cells/drug effects ; Endothelial Cells/enzymology ; Endothelial Cells/metabolism ; Focal Adhesions/drug effects ; Focal Adhesions/metabolism ; Glioblastoma/drug therapy ; Glioblastoma/pathology ; Humans ; Jurkat Cells ; Mice, Inbred C57BL ; Phosphorylation/drug effects ; Receptors, Adenosine A2/metabolism ; Signal Transduction/drug effects ; Stress Fibers/drug effects ; Stress Fibers/metabolism ; T-Lymphocytes/cytology ; T-Lymphocytes/drug effects ; Tight Junctions/drug effects ; Tight Junctions/metabolism ; rhoA GTP-Binding Protein/metabolism
Chemical Substances	Adenosine A2 Receptor Agonists ; Antineoplastic Agents ; Receptors, Adenosine A2 ; Deoxycytidine (0W860991D6) ; gemcitabine (B76N6SBZ8R) ; rhoA GTP-Binding Protein (EC 3.6.5.2)
Language	English
Publishing date	2014-09-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-014-8879-2
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Article ; Online: Thrombin induces an inflammatory phenotype in a human brain endothelial cell line.

Alabanza, Leah M / Bynoe, Margaret S

Journal of neuroimmunology

2012 Volume 245, Issue 1-2, Page(s) 48–55

Abstract: In this study, we utilized the human brain endothelial cell line, hCMEC/D3, to determine the effects of the coagulation factor, thrombin, on the human blood-brain barrier (BBB). We show that thrombin increased the mRNA and cell surface levels of ICAM-1 ... ...

Abstract	In this study, we utilized the human brain endothelial cell line, hCMEC/D3, to determine the effects of the coagulation factor, thrombin, on the human blood-brain barrier (BBB). We show that thrombin increased the mRNA and cell surface levels of ICAM-1 and VCAM-1 in hCMEC/D3 cells. Thrombin similarly upregulated several chemokines implicated in human neurological conditions. Additionally, the paracellular permeability of the human BBB in vitro was also increased following thrombin treatment. Overall, this study demonstrates that thrombin can effectively induce an inflamed phenotype in an in vitro human BBB.
MeSH term(s)	Blood-Brain Barrier/immunology ; Blood-Brain Barrier/metabolism ; Blood-Brain Barrier/pathology ; Cell Adhesion/drug effects ; Cell Adhesion/immunology ; Cell Line ; Endothelial Cells/immunology ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Humans ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/metabolism ; Inflammation Mediators/toxicity ; Phenotype ; Thrombin/toxicity
Chemical Substances	Inflammation Mediators ; Thrombin (EC 3.4.21.5)
Language	English
Publishing date	2012-02-29
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	8335-5
ISSN	1872-8421 ; 0165-5728
ISSN (online)	1872-8421
ISSN	0165-5728
DOI	10.1016/j.jneuroim.2012.02.004
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Article ; Online: CD73-generated adenosine is critical for immune regulation during Toxoplasma gondii infection.

Mahamed, Deeqa A / Toussaint, Leon E / Bynoe, Margaret S

Infection and immunity

2015 Volume 83, Issue 2, Page(s) 721–729

Abstract: As an obligate intracellular pathogen, the apicomplexan parasite Toxoplasma gondii evades immune system-mediated clearance by undergoing stage differentiation to persist indefinitely in susceptible hosts. Previously, we found that mice deficient in the ... ...

Abstract	As an obligate intracellular pathogen, the apicomplexan parasite Toxoplasma gondii evades immune system-mediated clearance by undergoing stage differentiation to persist indefinitely in susceptible hosts. Previously, we found that mice deficient in the ectoenzyme CD73, which generates adenosine in the extracellular matrix, were resistant to chronic toxoplasmosis after oral infection with T. gondii. Resistance in CD73 knockout mice was due to a delay in parasite differentiation in the central nervous system (CNS). To further clarify the role of CD73 and extracellular adenosine in T. gondii pathogenesis, we infected wild-type (WT) and CD73(-/-) mice with T. gondii cysts systemically by the intraperitoneal (i.p.) route. In contrast to oral infection, i.p. infected CD73(-/-) mice were highly susceptible to immune-mediated pathology, with significantly increased infiltration of neutrophils and T cells into the peritoneal cavity. Administration of the broad-spectrum adenosine receptor agonist 5'-N-ethylcarboxamidoadenosine (NECA) protected CD73(-/-) mice against T. gondii-induced immunopathology, suggesting that the absence of CD73-generated adenosine led to the increased susceptibility in these mice. Peritoneal exudate cells from infected CD73(-/-) mice produced higher levels of the inflammatory mediators nitric oxide, tumor necrosis factor alpha (TNF-α), and interleukin-1β (IL-1β), without enhanced parasite killing or clearance. Bone marrow chimeras established that CD73 expression in both hematopoietic and nonhematopoietic compartments contributes to limiting T. gondii-induced immunopathology. In addition, mice deficient in the adenosine receptor A(2A) were more susceptible to immunopathology during intraperitoneal infection with T. gondii than WT mice. Thus, extracellular adenosine is a key immune regulator that limits collateral tissue damage due to an intracellular pathogen and promotes host survival.
MeSH term(s)	5'-Nucleotidase/genetics ; 5'-Nucleotidase/metabolism ; Adenosine/genetics ; Adenosine/immunology ; Adenosine-5'-(N-ethylcarboxamide)/pharmacology ; Animals ; Antineoplastic Agents/pharmacology ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/immunology ; Cells, Cultured ; Inflammation/genetics ; Inflammation/immunology ; Inflammation Mediators/blood ; Interleukin-1beta/blood ; Lymphocyte Activation/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neutrophil Infiltration/immunology ; Neutrophils/immunology ; Nitric Oxide/biosynthesis ; Purinergic P1 Receptor Agonists/pharmacology ; Toxoplasma/immunology ; Toxoplasmosis/immunology ; Tumor Necrosis Factor-alpha/blood
Chemical Substances	Antineoplastic Agents ; Inflammation Mediators ; Interleukin-1beta ; Purinergic P1 Receptor Agonists ; Tumor Necrosis Factor-alpha ; Nitric Oxide (31C4KY9ESH) ; Adenosine-5'-(N-ethylcarboxamide) (35920-39-9) ; 5'-Nucleotidase (EC 3.1.3.5) ; Adenosine (K72T3FS567)
Language	English
Publishing date	2015-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	218698-6
ISSN	1098-5522 ; 0019-9567
ISSN (online)	1098-5522
ISSN	0019-9567
DOI	10.1128/IAI.02536-14
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Article ; Online: Toxoplasma gondii alters NMDAR signaling and induces signs of Alzheimer's disease in wild-type, C57BL/6 mice.

Torres, Luisa / Robinson, Sudie-Ann / Kim, Do-Geun / Yan, Angela / Cleland, Thomas A / Bynoe, Margaret S

Journal of neuroinflammation

2018 Volume 15, Issue 1, Page(s) 57

Abstract: Background: Alzheimer's disease (AD) is a progressive neurodegenerative disease associated with cognitive decline and complete loss of basic functions. The ubiquitous apicomplexan parasite Toxoplasma gondii (T. gondii) infects up to one third of the ... ...

Abstract	Background: Alzheimer's disease (AD) is a progressive neurodegenerative disease associated with cognitive decline and complete loss of basic functions. The ubiquitous apicomplexan parasite Toxoplasma gondii (T. gondii) infects up to one third of the world's population and is implicated in AD. Methods: We infected C57BL/6 wild-type male and female mice with 10 T. gondii ME49 cysts and assessed whether infection led to behavioral and anatomical effects using immunohistochemistry, immunofluorescence, Western blotting, cell culture assays, as well as an array of mouse behavior tests. Results: We show that T. gondii infection induced two major hallmarks of AD in the brains of C57BL/6 male and female mice: beta-amyloid (Aβ) immunoreactivity and hyperphosphorylated Tau. Infected mice showed significant neuronal death, loss of N-methyl-D-aspartate receptor (NMDAR) expression, and loss of olfactory sensory neurons. T. gondii infection also caused anxiety-like behavior, altered recognition of social novelty, altered spatial memory, and reduced olfactory sensitivity. This last finding was exclusive to male mice, as infected females showed intact olfactory sensitivity. Conclusions: These results demonstrate that T. gondii can induce advanced signs of AD in wild-type mice and that it may induce AD in some individuals with underlying health problems.
MeSH term(s)	Alzheimer Disease/etiology ; Alzheimer Disease/metabolism ; Alzheimer Disease/parasitology ; Animals ; Cells, Cultured ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Random Allocation ; Receptors, N-Methyl-D-Aspartate/metabolism ; Signal Transduction/physiology ; Toxoplasma ; Toxoplasmosis/complications ; Toxoplasmosis/metabolism
Chemical Substances	Receptors, N-Methyl-D-Aspartate
Language	English
Publishing date	2018-02-23
Publishing country	England
Document type	Journal Article
ZDB-ID	2156455-3
ISSN	1742-2094 ; 1742-2094
ISSN (online)	1742-2094
ISSN	1742-2094
DOI	10.1186/s12974-018-1086-8
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Article ; Online: CD73 Promotes Glioblastoma Pathogenesis and Enhances Its Chemoresistance via A

Yan, Angela / Joachims, Michelle L / Thompson, Linda F / Miller, Andrew D / Canoll, Peter D / Bynoe, Margaret S

The Journal of neuroscience : the official journal of the Society for Neuroscience

2019 Volume 39, Issue 22, Page(s) 4387–4402

Abstract: Glioblastoma (GB) is one of the deadliest brain cancers to afflict humans, and it has a very poor survival rate even with treatment. The extracellular adenosine-generating enzyme CD73 is involved in many cellular functions that can be usurped by tumors, ... ...

Abstract	Glioblastoma (GB) is one of the deadliest brain cancers to afflict humans, and it has a very poor survival rate even with treatment. The extracellular adenosine-generating enzyme CD73 is involved in many cellular functions that can be usurped by tumors, including cell adhesion, proliferation, invasion, and angiogenesis. We set out to determine the role of CD73 in GB pathogenesis. To do this, we established a unique GB mouse model (CD73-FLK) in which we spatially expressed CD73 on endothelial cells in CD73
MeSH term(s)	5'-Nucleotidase/metabolism ; Animals ; Brain Neoplasms/metabolism ; Brain Neoplasms/pathology ; Drug Resistance, Neoplasm/physiology ; Glioblastoma/metabolism ; Glioblastoma/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Receptor, Adenosine A2B/metabolism ; Signal Transduction/physiology
Chemical Substances	Receptor, Adenosine A2B ; 5'-Nucleotidase (EC 3.1.3.5)
Language	English
Publishing date	2019-03-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.1118-18.2019
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Zs.A 1668: Show issues

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Article: Adenosine receptor signaling: a key to opening the blood-brain door.

Bynoe, Margaret S / Viret, Christophe / Yan, Angela / Kim, Do-Geun

Fluids and barriers of the CNS

2015 Volume 12, Page(s) 20

Abstract: The aim of this review is to outline evidence that adenosine receptor (AR) activation can modulate blood-brain barrier (BBB) permeability and the implications for disease states and drug delivery. Barriers of the central nervous system (CNS) constitute a ...

Abstract	The aim of this review is to outline evidence that adenosine receptor (AR) activation can modulate blood-brain barrier (BBB) permeability and the implications for disease states and drug delivery. Barriers of the central nervous system (CNS) constitute a protective and regulatory interface between the CNS and the rest of the organism. Such barriers allow for the maintenance of the homeostasis of the CNS milieu. Among them, the BBB is a highly efficient permeability barrier that separates the brain micro-environment from the circulating blood. It is made up of tight junction-connected endothelial cells with specialized transporters to selectively control the passage of nutrients required for neural homeostasis and function, while preventing the entry of neurotoxic factors. The identification of cellular and molecular mechanisms involved in the development and function of CNS barriers is required for a better understanding of CNS homeostasis in both physiological and pathological settings. It has long been recognized that the endogenous purine nucleoside adenosine is a potent modulator of a large number of neurological functions. More recently, experimental studies conducted with human/mouse brain primary endothelial cells as well as with mouse models, indicate that adenosine markedly regulates BBB permeability. Extracellular adenosine, which is efficiently generated through the catabolism of ATP via the CD39/CD73 ecto-nucleotidase axis, promotes BBB permeability by signaling through A1 and A2A ARs expressed on BBB cells. In line with this hypothesis, induction of AR signaling by selective agonists efficiently augments BBB permeability in a transient manner and promotes the entry of macromolecules into the CNS. Conversely, antagonism of AR signaling blocks the entry of inflammatory cells and soluble factors into the brain. Thus, AR modulation of the BBB appears as a system susceptible to tighten as well as to permeabilize the BBB. Collectively, these findings point to AR manipulation as a pertinent avenue of research for novel strategies aiming at efficiently delivering therapeutic drugs/cells into the CNS, or at restricting the entry of inflammatory immune cells into the brain in some diseases such as multiple sclerosis.
MeSH term(s)	Adenosine/metabolism ; Animals ; Blood-Brain Barrier/cytology ; Blood-Brain Barrier/metabolism ; Capillary Permeability ; Drug Delivery Systems ; Endothelial Cells/metabolism ; Humans ; Mice ; Neurons/metabolism ; Receptors, Purinergic P1/metabolism ; Signal Transduction
Chemical Substances	Receptors, Purinergic P1 ; Adenosine (K72T3FS567)
Language	English
Publishing date	2015-09-02
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2595406-4
ISSN	2045-8118
ISSN	2045-8118
DOI	10.1186/s12987-015-0017-7
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Article: Foxp3+CD4+ T cell-mediated immunosuppression involves extracellular nucleotide catabolism.

Bynoe, Margaret S / Viret, Christophe

Trends in immunology

2008 Volume 29, Issue 3, Page(s) 99–102

Abstract: Foxp3(+)CD4(+) T cells represent a population of naturally arising suppressor T cells that are crucial for the control of autoimmune responses. The suppressive activity of this T cell subset relies on multiple mechanisms that include secretion of anti- ... ...

Abstract	Foxp3(+)CD4(+) T cells represent a population of naturally arising suppressor T cells that are crucial for the control of autoimmune responses. The suppressive activity of this T cell subset relies on multiple mechanisms that include secretion of anti-inflammatory factors such as TGF-beta or IL-10. Novel studies now establish that, through the generation of the immunosuppressive factor adenosine, the ectoenzymes CD39 and CD73 are important contributors to the regulatory activity of Foxp3(+)CD4(+) T cells.
MeSH term(s)	Animals ; Extracellular Space/immunology ; Extracellular Space/metabolism ; Forkhead Transcription Factors/biosynthesis ; Humans ; Immune Tolerance/immunology ; Mice ; Nucleotides/metabolism ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism
Chemical Substances	FOXP3 protein, human ; Forkhead Transcription Factors ; Foxp3 protein, mouse ; Nucleotides
Language	English
Publishing date	2008-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2036831-8
ISSN	1471-4981 ; 1471-4906
ISSN (online)	1471-4981
ISSN	1471-4906
DOI	10.1016/j.it.2007.12.005
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Zs.A 1601: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Itk signals promote neuroinflammation by regulating CD4+ T-cell activation and trafficking.

Kannan, Arun K / Kim, Do-Geun / August, Avery / Bynoe, Margaret S

The Journal of neuroscience : the official journal of the Society for Neuroscience

2014 Volume 35, Issue 1, Page(s) 221–233

Abstract: Here we demonstrate that interleukin-2-inducible T-cell kinase (Itk) signaling in cluster of differentiation 4-positive (CD4(+)) T cells promotes experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis (MS). We show that ... ...

Abstract	Here we demonstrate that interleukin-2-inducible T-cell kinase (Itk) signaling in cluster of differentiation 4-positive (CD4(+)) T cells promotes experimental autoimmune encephalomyelitis (EAE), the animal model of multiple sclerosis (MS). We show that Itk(-/-) mice exhibit reduced disease severity, and transfer of Itk(-/-) CD4(+) T cells into T cell-deficient recipients results in lower disease severity. We observed a significant reduction of CD4(+) T cells in the CNS of Itk(-/-) mice or recipients of Itk(-/-) CD4(+) T cells during EAE, which is consistent with attenuated disease. Itk(-/-) CD4(+) T cells exhibit defective response to myelin antigen stimulation attributable to displacement of filamentous actin from the CD4(+) coreceptor. This results in inadequate transmigration of Itk(-/-) CD4(+) T cells into the CNS and across brain endothelial barriers in vitro. Finally, Itk(-/-) CD4(+) T cells show significant reduction in production of T-helper 1 (Th1) and Th17 cytokines and exhibit skewed T effector/T regulatory cell ratios. These results indicate that signaling by Itk promotes autoimmunity and CNS inflammation, suggesting that it may be a viable target for treatment of MS.
MeSH term(s)	Animals ; CD4-Positive T-Lymphocytes/metabolism ; Cell Movement/physiology ; Encephalomyelitis, Autoimmune, Experimental/metabolism ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Female ; Inflammation/metabolism ; Inflammation/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Protein Transport/physiology ; Protein-Tyrosine Kinases/metabolism ; Signal Transduction/physiology
Chemical Substances	Protein-Tyrosine Kinases (EC 2.7.10.1) ; emt protein-tyrosine kinase (EC 2.7.10.2)
Language	English
Publishing date	2014-12-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.1957-14.2015
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