Human autoimmunity after lymphocyte depletion is caused by homeostatic T-cell proliferation. - Wikidata - wikimedia - TriplyDB

Human autoimmunity after lymphocyte depletion is caused by homeostatic T-cell proliferation.

Human autoimmunity after lymphocyte depletion is caused by homeostatic T-cell proliferation.

http://www.wikidata.org/entity/Q37395089

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High-throughput sequencing of immune repertoires in multiple sclerosis Alemtuzumab in Multiple Sclerosis: Mechanism of Action and Beyond Alemtuzumab in the treatment of multiple sclerosis: key clinical trial results and considerations for use Alemtuzumab for Multiple Sclerosis.Alemtuzumab in the treatment of multiple sclerosis: patient selection and special considerations Alemtuzumab for the treatment of multiple sclerosis The orally available, synthetic ether lipid edelfosine inhibits T cell proliferation and induces a type I interferon response Occurrence of Anti-Drug Antibodies against Interferon-Beta and Natalizumab in Multiple Sclerosis: A Collaborative Cohort Analysis Progressive multi-focal leucoencephalopathy - driven from rarity to clinical mainstream by iatrogenic immunodeficiency.Alemtuzumab for the treatment of relapsing-remitting multiple sclerosis: a review of its clinical pharmacology, efficacy and safety.Neuroimmunotherapies Targeting T Cells: From Pathophysiology to Therapeutic Applications.Accelerated lymphocyte recovery after alemtuzumab does not predict multiple sclerosis activity.Lipid-specific immunoglobulin M bands in cerebrospinal fluid are associated with a reduced risk of developing progressive multifocal leukoencephalopathy during treatment with natalizumab.Haematopoietic stem cell transplantation for autoimmune diseases.Diversity and clonal selection in the human T-cell repertoire.Hyperexpansion of Functional Viral-Specific CD8+ T Cells in Lymphopenia-Associated MCMV Pneumonitis.T cells in the control of organ-specific autoimmunity ALAIN01--Alemtuzumab in autoimmune inflammatory neurodegeneration: mechanisms of action and neuroprotective potential.Interpreting Lymphocyte Reconstitution Data From the Pivotal Phase 3 Trials of Alemtuzumab.Bystander hyperactivation of preimmune CD8+ T cells in chronic HCV patients Suppression of IL-7-dependent Effector T-cell Expansion by Multipotent Adult Progenitor Cells and PGE2.Decreases in thymopoiesis of astronauts returning from space flight.An observational study of alemtuzumab following fingolimod for multiple sclerosis.Alemtuzumab: a review of its use in patients with relapsing multiple sclerosis.Optimized nonclinical safety assessment strategies supporting clinical development of therapeutic monoclonal antibodies targeting inflammatory diseases.Homeostatic expansion as a barrier to lymphocyte depletion strategies.Drug safety evaluation of alemtuzumab for multiple sclerosis.Alemtuzumab: a new therapy for active relapsing-remitting multiple sclerosis.Both cladribine and alemtuzumab may effect MS via B-cell depletion Monoclonal Antibodies for Relapsing Multiple Sclerosis: A Review of Recently Marketed and Late-Stage Agents.Neonatal and adult recent thymic emigrants produce IL-8 and express complement receptors CR1 and CR2.Multifunctional roles of the autoimmune disease-associated tyrosine phosphatase PTPN22 in regulating T cell homeostasis.Clonal and constricted T cell repertoire in Common Variable Immune Deficiency.The tyrosine phosphatase PTPN22 discriminates weak self peptides from strong agonist TCR signals.CD275-Independent IL-17-Producing T Follicular Helper-like Cells in Lymphopenic Autoimmune-Prone Mice.Reconstitution of the peripheral immune repertoire following withdrawal of fingolimod.B cells in type 1 diabetes mellitus and diabetic kidney disease.Depletion-Resistant CD4 T Cells Enhance Thymopoiesis During Lymphopenia.Regenerating Immunotolerance in Multiple Sclerosis with Autologous Hematopoietic Stem Cell Transplant.The microbiome and autoimmunity: a paradigm from the gut-liver axis.

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Human autoimmunity after lymphocyte depletion is caused by homeostatic T-cell proliferation.

http://www.wikidata.org/entity/Q37395089

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2013 nî lūn-bûn

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2013年学术文章

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2013年學術文章

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2013年學術文章

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2013年學術文章

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name

Human autoimmunity after lymph ...... eostatic T-cell proliferation.

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Human autoimmunity after lymph ...... eostatic T-cell proliferation.

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Human autoimmunity after lymph ...... eostatic T-cell proliferation.

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Human autoimmunity after lymph ...... eostatic T-cell proliferation.

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Human autoimmunity after lymph ...... eostatic T-cell proliferation.

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Human autoimmunity after lymph ...... eostatic T-cell proliferation.

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PNAS.1313654110

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Proceedings of the National Academy of Sciences of the United States of America

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Human autoimmunity after lymph ...... eostatic T-cell proliferation.

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Alasdair J Coles

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Allison J Curry

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Jessica L Davies

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Joanne L Jones

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Laura Azzopardi

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Orla C Tuohy

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Priscilla Loh

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Sara A J Thompson

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P2860

Expression of CD57 defines replicative senescence and antigen-induced apoptotic death of CD8+ T cells

Alemtuzumab for patients with relapsing multiple sclerosis after disease-modifying therapy: a randomised controlled phase 3 trial

Adenosine generation catalyzed by CD39 and CD73 expressed on regulatory T cells mediates immune suppression.

T cell exhaustion

Alemtuzumab versus interferon beta 1a as first-line treatment for patients with relapsing-remitting multiple sclerosis: a randomised controlled phase 3 trial

Analysis of T-cell repertoire diversity in Wiskott-Aldrich syndrome.

Alemtuzumab vs. interferon beta-1a in early multiple sclerosis.

Homeostatic expansion of T cells during immune insufficiency generates autoimmunity.

Helios expression is a marker of T cell activation and proliferation.

Cutting edge: depletion of CD4+CD25+ regulatory T cells is necessary, but not sufficient, for induction of organ-specific autoimmune disease.

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20200-20205

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10.1073/PNAS.1313654110

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50

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110

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Alastair Compston

Grant A Hill-Cawthorne

Michael T Fahey

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2013-11-26T00:00:00Z

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258955696

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24282306

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3864306

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