An unexpected version of horror autotoxicus: anaphylactic shock to a self-peptide. - Wikidata - awgldk - TriplyDB

An unexpected version of horror autotoxicus: anaphylactic shock to a self-peptide.

An unexpected version of horror autotoxicus: anaphylactic shock to a self-peptide.

http://www.wikidata.org/entity/Q32063760

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T cell recognition of weak ligands: roles of signaling, receptor number, and affinity Severe anaphylactic reactions to glutamic acid decarboxylase (GAD) self peptides in NOD mice that spontaneously develop autoimmune type 1 diabetes mellitus The Role of Chemokines in Shaping the Balance Between CD4(+) T Cell Subsets and Its Therapeutic Implications in Autoimmune and Cancer Diseases Tempering allorecognition to induce transplant tolerance with chemically modified apoptotic donor cells Instant effect of soluble antigen on effector T cells in peripheral immune organs during immunotherapy of autoimmune encephalomyelitis A GMCSF-neuroantigen fusion protein is a potent tolerogen in experimental autoimmune encephalomyelitis (EAE) that is associated with efficient targeting of neuroantigen to APC Molecular mechanisms of T-cell receptor and costimulatory molecule ligation/blockade in autoimmune disease therapy.Therapeutic blockade of T-cell antigen receptor signal transduction and costimulation in autoimmune disease Manipulating antigenic ligand strength to selectively target myelin-reactive CD4+ T cells in EAE.Differential induction of IgE-mediated anaphylaxis after soluble vs. cell-bound tolerogenic peptide therapy of autoimmune encephalomyelitis.'Multi-epitope-targeted' immune-specific therapy for a multiple sclerosis-like disease via engineered multi-epitope protein is superior to peptides Mast cells in autoimmune disease.Sequential transcriptional changes dictate safe and effective antigen-specific immunotherapy.Immunogenicity to biologics: mechanisms, prediction and reduction.Myelin-specific CD8 T cells in the pathogenesis of experimental allergic encephalitis and multiple sclerosis.Peptide-based immunotherapy of autoimmunity: a path of puzzles, paradoxes and possibilities.Antigen-presenting cells and tolerance induction.Multiple elements of the allergic arm of the immune response modulate autoimmune demyelination.Anti-peptide autoantibodies and fatal anaphylaxis in NOD mice in response to insulin self-peptides B:9-23 and B:13-23 Antigen-based immune modulation: DNA vectors and beyond.Attenuation of Th1 effector cell responses and susceptibility to experimental allergic encephalomyelitis in histamine H2 receptor knockout mice is due to dysregulation of cytokine production by antigen-presenting cells.Gene therapy in autoimmune, demyelinating disease of the central nervous system.Dominant role of antigen dose in CD4+Foxp3+ regulatory T cell induction and expansion.Preclinical development and first-in-human study of ATX-MS-1467 for immunotherapy of MS Critical role for prokineticin 2 in CNS autoimmunity.Antigen-specific blocking of CD4-specific immunological synapse formation using BPI and current therapies for autoimmune diseases.Preferential Interactions and the Effect of Protein PEGylation.Multi-peptide coupled-cell tolerance ameliorates ongoing relapsing EAE associated with multiple pathogenic autoreactivities.Multimerized T cell epitopes protect from experimental autoimmune diabetes by inducing dominant tolerance.Mast Cells are Important Modifiers of Autoimmune Disease: With so Much Evidence, Why is There Still Controversy?Immune modulating peptides for the treatment and suppression of multiple sclerosis.Targeting the TCR: T-cell receptor and peptide-specific tolerance-based strategies for restoring self-tolerance in CNS autoimmune disease.Optic neuritis, a new variant of experimental encephalomyelitis, a durable model for all seasons, now in its seventieth year.Dual phase regulation of experimental allergic encephalomyelitis by platelet-activating factor.Endogenous erythropoietin as part of the cytokine network in the pathogenesis of experimental autoimmune encephalomyelitis.Reversal of paralysis and reduced inflammation from peripheral administration of β-amyloid in TH1 and TH17 versions of experimental autoimmune encephalomyelitis.Prophylactic and therapeutic suppression of experimental autoimmune encephalomyelitis by a novel bifunctional peptide inhibitor.A Journey in Science: The Privilege of Exploring the Brain and the Immune System.Peptide-based immunotherapy of experimental autoimmune encephalomyelitis without anaphylaxis.L.E.A.P.S. heteroconjugate is able to prevent and treat experimental autoimmune myocarditis by altering trafficking of autoaggressive cells to the heart.

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An unexpected version of horror autotoxicus: anaphylactic shock to a self-peptide.

http://www.wikidata.org/entity/Q32063760

description

2001 nî lūn-bûn

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2001 թուականի Մարտին հրատարակուած գիտական յօդուած

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2001 թվականի մարտին հրատարակված գիտական հոդված

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2001年の論文

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2001年論文

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2001年論文

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2001年論文

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2001年論文

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2001年論文

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2001年论文

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name

An unexpected version of horror autotoxicus: anaphylactic shock to a self-peptide.

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An unexpected version of horror autotoxicus: anaphylactic shock to a self-peptide.

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type

label

An unexpected version of horror autotoxicus: anaphylactic shock to a self-peptide.

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An unexpected version of horror autotoxicus: anaphylactic shock to a self-peptide.

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An unexpected version of horror autotoxicus: anaphylactic shock to a self-peptide.

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An unexpected version of horror autotoxicus: anaphylactic shock to a self-peptide.

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Nature Immunology

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An unexpected version of horror autotoxicus: anaphylactic shock to a self-peptide.

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Chabas D

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Galli SJ

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Hattab EM

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Karpuj M

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Mitchell D

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Pedotti R

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Steinman L

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Tsai M

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Wedemeyer J

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P2860

The human myelin basic protein gene is included within a 179-kilobase transcription unit: expression in the immune and central nervous systems

Functional diversity of helper T lymphocytes

Autoimmunity can benefit self-maintenance.

Regulation of the immune response to peptide antigens: differential induction of immediate-type hypersensitivity and T cell proliferation due to changes in either peptide structure or major histocompatibility complex haplotype

Acute autoimmune encephalomyelitis in mice. II. Susceptibility is controlled by the combination of H-2 and histamine sensitization genes

Prevention of autoimmune diabetes in non-obese diabetic mice by treatment with a class II major histocompatibility complex-blocking peptide.

Mast cells can amplify airway reactivity and features of chronic inflammation in an asthma model in mice.

Mast cells are essential for early onset and severe disease in a murine model of multiple sclerosis.

High frequency of autoreactive myelin proteolipid protein-specific T cells in the periphery of naive mice: mechanisms of selection of the self-reactive repertoire.

Myelin basic protein-specific T helper 2 (Th2) cells cause experimental autoimmune encephalomyelitis in immunodeficient hosts rather than protect them from the disease.

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216-222

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3

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11224520

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