scholarly article | Q13442814 |
P50 | author | Vijay Kuchroo | Q87889159 |
P2093 | author name string | Sheng Xiao | |
Raymond A Sobel | |||
Youjin Lee | |||
Meike Mitsdoerffer | |||
Guangxiang Gu | |||
P2860 | cites work | The interleukin 23 receptor is essential for the terminal differentiation of interleukin 17-producing effector T helper cells in vivo | Q24600773 |
Generation of pathogenic T(H)17 cells in the absence of TGF-β signalling | Q24625230 | ||
Th17 and regulatory T cells in mediating and restraining inflammation | Q27687428 | ||
Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells | Q27860460 | ||
IL-17 and Th17 Cells | Q27860566 | ||
The orphan nuclear receptor RORgammat directs the differentiation program of proinflammatory IL-17+ T helper cells | Q27860620 | ||
Transforming growth factor-beta induces development of the T(H)17 lineage | Q28237370 | ||
The nature of multiple sclerosis | Q28264847 | ||
IL-23 drives a pathogenic T cell population that induces autoimmune inflammation | Q29547525 | ||
Interleukin-23 rather than interleukin-12 is the critical cytokine for autoimmune inflammation of the brain | Q29614225 | ||
Animal models of multiple sclerosis | Q71731098 | ||
Neuropathology in multiple sclerosis: new concepts | Q77377209 | ||
IL-17 plays an important role in the development of experimental autoimmune encephalomyelitis | Q79755041 | ||
IL-6 programs T(H)-17 cell differentiation by promoting sequential engagement of the IL-21 and IL-23 pathways | Q29614839 | ||
Essential autocrine regulation by IL-21 in the generation of inflammatory T cells | Q29616147 | ||
IL-21 initiates an alternative pathway to induce proinflammatory T(H)17 cells | Q29616148 | ||
Interleukin-22, a T(H)17 cytokine, mediates IL-23-induced dermal inflammation and acanthosis | Q29620506 | ||
IL-21 limits peripheral lymphocyte numbers through T cell homeostatic mechanisms | Q33367125 | ||
IL-21 regulates germinal center B cell differentiation and proliferation through a B cell-intrinsic mechanism | Q33656121 | ||
IL-21 acts directly on B cells to regulate Bcl-6 expression and germinal center responses | Q33656146 | ||
Homeostatic expansion of T cells during immune insufficiency generates autoimmunity. | Q33977505 | ||
Proinflammatory T helper type 17 cells are effective B-cell helpers | Q34069686 | ||
T cell response in experimental autoimmune encephalomyelitis (EAE): role of self and cross-reactive antigens in shaping, tuning, and regulating the autopathogenic T cell repertoire | Q34542240 | ||
B cells move to centre stage: novel opportunities for autoimmune disease treatment | Q34544062 | ||
RORγt drives production of the cytokine GM-CSF in helper T cells, which is essential for the effector phase of autoimmune neuroinflammation. | Q34660473 | ||
IL-21 signaling is critical for the development of type I diabetes in the NOD mouse | Q34823699 | ||
Myelin oligodendrocyte glycoprotein-specific T and B cells cooperate to induce a Devic-like disease in mice | Q35009518 | ||
Fulminant spontaneous autoimmunity of the central nervous system in mice transgenic for the myelin proteolipid protein-specific T cell receptor | Q35111360 | ||
Differential IL-21 signaling in APCs leads to disparate Th17 differentiation in diabetes-susceptible NOD and diabetes-resistant NOD.Idd3 mice. | Q35484777 | ||
Induction and molecular signature of pathogenic TH17 cells | Q36283752 | ||
Myelin oligodendrocyte glycoprotein-specific T cell receptor transgenic mice develop spontaneous autoimmune optic neuritis. | Q36370963 | ||
CCR6 is required for epidermal trafficking of γδ-T cells in an IL-23-induced model of psoriasiform dermatitis | Q36438118 | ||
Neuromyelitis optica - Devic's syndrome, update | Q36617526 | ||
IL-6 controls Th17 immunity in vivo by inhibiting the conversion of conventional T cells into Foxp3+ regulatory T cells | Q36985100 | ||
Interleukin-21 is required for the development of type 1 diabetes in NOD mice | Q37163453 | ||
MHC class II-dependent B cell APC function is required for induction of CNS autoimmunity independent of myelin-specific antibodies | Q37397820 | ||
Animal models of multiple sclerosis | Q37451051 | ||
IL-17RC is required for IL-17A- and IL-17F-dependent signaling and the pathogenesis of experimental autoimmune encephalomyelitis. | Q39727345 | ||
Targeting Th17 cells in immune diseases | Q41827404 | ||
Interleukin-23 drives intestinal inflammation through direct activity on T cells | Q42083897 | ||
Transgenic mice that express a myelin basic protein-specific T cell receptor develop spontaneous autoimmunity | Q43433033 | ||
IL-21 and IL-21R are not required for development of Th17 cells and autoimmunity in vivo | Q46546464 | ||
Neutralizing antibodies to IFN-gamma-inducing factor prevent experimental autoimmune encephalomyelitis | Q48339467 | ||
Pathogen-induced human TH17 cells produce IFN-γ or IL-10 and are regulated by IL-1β. | Q50959906 | ||
Mice with a disrupted IFN-gamma gene are susceptible to the induction of experimental autoimmune encephalomyelitis (EAE). | Q52519041 | ||
Transforming growth factor-beta 'reprograms' the differentiation of T helper 2 cells and promotes an interleukin 9-producing subset. | Q53446140 | ||
Signals mediated by transforming growth factor-beta initiate autoimmune encephalomyelitis, but chronic inflammation is needed to sustain disease. | Q53597450 | ||
The N-terminal domain of the myelin oligodendrocyte glycoprotein (MOG) induces acute demyelinating experimental autoimmune encephalomyelitis in the Lewis rat | Q61709774 | ||
Conditional DC depletion does not affect priming of encephalitogenic Th cells in EAE | Q61960513 | ||
Cutting Edge: IL-21 Is Not Essential for Th17 Differentiation or Experimental Autoimmune Encephalomyelitis | Q62230222 | ||
Immunogenic and encephalitogenic epitope clusters of myelin proteolipid protein | Q63535313 | ||
Identification and characterization of a second encephalitogenic determinant of myelin proteolipid protein (residues 178-191) for SJL mice | Q63535319 | ||
IFN-gamma plays a critical down-regulatory role in the induction and effector phase of myelin oligodendrocyte glycoprotein-induced autoimmune encephalomyelitis | Q71687717 | ||
P433 | issue | 11 | |
P407 | language of work or name | English | Q1860 |
P921 | main subject | experimental autoimmune encephalomyelitis | Q494066 |
P304 | page(s) | 4011-4020 | |
P577 | publication date | 2015-09-28 | |
P1433 | published in | Journal of Clinical Investigation | Q3186904 |
P1476 | title | IL-21R signaling is critical for induction of spontaneous experimental autoimmune encephalomyelitis | |
P478 | volume | 125 |
Q36600988 | A Context-Dependent Role for IL-21 in Modulating the Differentiation, Distribution, and Abundance of Effector and Memory CD8 T Cell Subsets. |
Q48065880 | CTL-Promoting Effects of IL-21 Counteract Murine Lupus in the Parent→F1 Graft-versus-Host Disease Model |
Q64962012 | Defective IgA response to atypical intestinal commensals in IL-21 receptor deficiency reshapes immune cell homeostasis and mucosal immunity. |
Q38961438 | Deficiency of the immunostimulatory cytokine IL-21 promotes intestinal neoplasia via dysregulation of the Th1/Th17 axis. |
Q57810320 | Emerging Role of Follicular T Helper Cells in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis |
Q38889721 | IL-21 and T Cell Differentiation: Consider the Context |
Q64953106 | IL-21 receptor signaling is essential for control of hepatocellular carcinoma growth and immunological memory for tumor challenge. |
Q90414688 | Identification of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome-associated DNA methylation patterns |
Q37144124 | Interleukin-21 is associated with the severity of psoriasis vulgaris through promoting CD4+ T cells to differentiate into Th17 cells |
Q41660408 | Monoclonal Antibodies in Preclinical EAE Models of Multiple Sclerosis: A Systematic Review |
Q38765404 | Th17 cells in neuromyelitis optica spectrum disorder: a review |
Q50175862 | The Interleukin (IL)-23/T helper (Th)17 Axis in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis |
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