Reversal of spontaneous autoimmune insulitis in nonobese diabetic mice by soluble lymphotoxin receptor. - Wikidata - awgldk - TriplyDB

Reversal of spontaneous autoimmune insulitis in nonobese diabetic mice by soluble lymphotoxin receptor.

Reversal of spontaneous autoimmune insulitis in nonobese diabetic mice by soluble lymphotoxin receptor.

http://www.wikidata.org/entity/Q36369174

about

The Lymphotoxin Network: orchestrating a type I interferon response to optimize adaptive immunity Stromal cell regulation of homeostatic and inflammatory lymphoid organogenesis Stromal Fibroblasts in Tertiary Lymphoid Structures: A Novel Target in Chronic Inflammation Endogenous association of TRAF2, TRAF3, cIAP1, and Smac with lymphotoxin beta receptor reveals a novel mechanism of apoptosis The central role of antigen presentation in islets of Langerhans in autoimmune diabetes Immunotherapy of type 1 diabetes: lessons for other autoimmune diseases.Multiple roles for tumor necrosis factor-alpha and lymphotoxin alpha/beta in immunity and autoimmunity.Herpesvirus entry mediator (TNFRSF14) regulates the persistence of T helper memory cell populations.CCR7 directs the recruitment of T cells into inflamed pancreatic islets of nonobese diabetic (NOD) mice.Myeloid-derived suppressor cells prevent type 1 diabetes in murine models Innate lymphotoxin receptor mediated signaling promotes HSV-1 associated neuroinflammation and viral replication.A role for surface lymphotoxin in experimental autoimmune encephalomyelitis independent of LIGHT.Transgenic LacZ under control of Hec-6st regulatory sequences recapitulates endogenous gene expression on high endothelial venules.Tumor-specific T cells signal tumor destruction via the lymphotoxin beta receptor Tolerance and lymphoid organ structure and function.Lymphotoxin and LIGHT signaling pathways and target genes.Differentiation and transplantation of functional pancreatic beta cells generated from induced pluripotent stem cells derived from a type 1 diabetes mouse model.CD25+ CD4+ T cells, expanded with dendritic cells presenting a single autoantigenic peptide, suppress autoimmune diabetes.Transgenic expression of decoy receptor 3 protects islets from spontaneous and chemical-induced autoimmune destruction in nonobese diabetic mice.Dysregulated LIGHT expression on T cells mediates intestinal inflammation and contributes to IgA nephropathy Differential regulation of CCL21 in lymphoid/nonlymphoid tissues for effectively attracting T cells to peripheral tissues.All-trans retinoic acid inhibits type 1 diabetes by T regulatory (Treg)-dependent suppression of interferon-gamma-producing T-cells without affecting Th17 cells.Cytokine related therapies for autoimmune disease Blockade of lymphotoxin-beta receptor signaling reduces aspects of Sjögren's syndrome in salivary glands of non-obese diabetic mice LIGHT/TNFSF14 is increased in patients with type 2 diabetes mellitus and promotes islet cell dysfunction and endothelial cell inflammation in vitro.LIGHT/IFN-γ triggers β cells apoptosis via NF-κB/Bcl2-dependent mitochondrial pathway.CXCL13 blockade disrupts B lymphocyte organization in tertiary lymphoid structures without altering B cell receptor bias or preventing diabetes in nonobese diabetic mice Mouse models for the study of autoimmune type 1 diabetes: a NOD to similarities and differences to human disease.LTβR and CD40: working together in dendritic cells to optimize immune responses.Lymphotoxin signalling in tertiary lymphoid structures and immunotherapy.Turning on LIGHT.A Lymphotoxin/Type I IFN Axis Programs CD8+ T Cells To Infiltrate a Self-Tissue and Propagate Immunopathology.Lymphotoxin pathway directs thymic Aire expression.Induction and effector phase of allergic lung inflammation is independent of CCL21/CCL19 and LT-beta.Manifestation of spontaneous and early autoimmune gastritis in CCR7-deficient mice Effects of streptozotocin on autoimmune diabetes in NOD mice.Resident fibroblasts in the kidney: a major driver of fibrosis and inflammation.Positioning of follicular dendritic cells within the spleen controls prion neuroinvasion

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P2860

Reversal of spontaneous autoimmune insulitis in nonobese diabetic mice by soluble lymphotoxin receptor.

http://www.wikidata.org/entity/Q36369174

description

2001 nî lūn-bûn

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2001年の論文

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2001年学术文章

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2001年学术文章

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2001年学术文章

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2001年学术文章

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2001年学术文章

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2001年學術文章

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2001年學術文章

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2001年學術文章

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Reversal of spontaneous autoim ...... soluble lymphotoxin receptor.

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Reversal of spontaneous autoim ...... soluble lymphotoxin receptor.

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Reversal of spontaneous autoim ...... soluble lymphotoxin receptor.

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Reversal of spontaneous autoim ...... soluble lymphotoxin receptor.

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Reversal of spontaneous autoim ...... soluble lymphotoxin receptor.

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Journal of Experimental Medicine

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Reversal of spontaneous autoim ...... soluble lymphotoxin receptor.

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B Salomon

http://www.w3.org/2001/XMLSchema#string

J A Bluestone

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L M Hoffman

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M Chen

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Q Wu

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Y Wang

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Y X Fu

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P2860

B7/CD28 costimulation is essential for the homeostasis of the CD4+CD25+ immunoregulatory T cells that control autoimmune diabetes

Characterization of lymphotoxin-alpha beta complexes on the surface of mouse lymphocytes

Development and maturation of secondary lymphoid tissues.

Tumor necrosis factor-alpha and the progression of diabetes in non-obese diabetic mice.

The NOD mouse model of type 1 diabetes: as good as it gets?

Complexities of CD28/B7: CTLA-4 costimulatory pathways in autoimmunity and transplantation.

The nonobese diabetic mouse as a model of autoimmune diabetes: immune dysregulation gets the NOD.

Lymphotoxin alpha/beta and tumor necrosis factor are required for stromal cell expression of homing chemokines in B and T cell areas of the spleen

The requirement of membrane lymphotoxin for the presence of dendritic cells in lymphoid tissues.

Lymphotoxin-alpha (LTalpha) supports development of splenic follicular structure that is required for IgG responses.

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11390440

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2193383

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