TCR Signaling Abnormalities in Human Th2-Associated Atopic Disease

Stimulation of naïve CD4 T cells with weak T cell receptor agonists even in the absence of T helper-skewing cytokines can result in IL-4 production which can drive a Th2 response. Evidence for the consequences of such a phenomenon can be found in a number of mouse models and, importantly, a series o...

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Published inFrontiers in immunology Vol. 9; p. 719
Main Author Milner, Joshua D.
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 16.04.2018
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ISSN1664-3224
1664-3224
DOI10.3389/fimmu.2018.00719

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Abstract Stimulation of naïve CD4 T cells with weak T cell receptor agonists even in the absence of T helper-skewing cytokines can result in IL-4 production which can drive a Th2 response. Evidence for the consequences of such a phenomenon can be found in a number of mouse models and, importantly, a series of monogenic human diseases associated with significant atopy which are caused by mutations in the T cell receptor signaling cascade. Such diseases can help understand how Th2 responses evolve in humans, and potentially provide insight into therapeutic interventions.
AbstractList Stimulation of naïve CD4 T cells with weak T cell receptor agonists even in the absence of T helper-skewing cytokines can result in IL-4 production which can drive a Th2 response. Evidence for the consequences of such a phenomenon can be found in a number of mouse models and, importantly, a series of monogenic human diseases associated with significant atopy which are caused by mutations in the T cell receptor signaling cascade. Such diseases can help understand how Th2 responses evolve in humans, and potentially provide insight into therapeutic interventions.
Stimulation of naïve CD4 T cells with weak T cell receptor agonists even in the absence of T helper-skewing cytokines can result in IL-4 production which can drive a Th2 response. Evidence for the in vivo consequences of such a phenomenon can be found in a number of mouse models and, importantly, a series of monogenic human diseases associated with significant atopy which are caused by mutations in the T cell receptor signaling cascade. Such diseases can help understand how Th2 responses evolve in humans, and potentially provide insight into therapeutic interventions.Stimulation of naïve CD4 T cells with weak T cell receptor agonists even in the absence of T helper-skewing cytokines can result in IL-4 production which can drive a Th2 response. Evidence for the in vivo consequences of such a phenomenon can be found in a number of mouse models and, importantly, a series of monogenic human diseases associated with significant atopy which are caused by mutations in the T cell receptor signaling cascade. Such diseases can help understand how Th2 responses evolve in humans, and potentially provide insight into therapeutic interventions.
Stimulation of naïve CD4 T cells with weak T cell receptor agonists even in the absence of T helper-skewing cytokines can result in IL-4 production which can drive a Th2 response. Evidence for the in vivo consequences of such a phenomenon can be found in a number of mouse models and, importantly, a series of monogenic human diseases associated with significant atopy which are caused by mutations in the T cell receptor signaling cascade. Such diseases can help understand how Th2 responses evolve in humans, and potentially provide insight into therapeutic interventions.
Stimulation of naïve CD4 T cells with weak T cell receptor agonists even in the absence of T helper-skewing cytokines can result in IL-4 production which can drive a Th2 response. Evidence for the in vivo consequences of such a phenomenon can be found in a number of mouse models and, importantly, a series of monogenic human diseases associated with significant atopy which are caused by mutations in the T cell receptor signaling cascade. Such diseases can help understand how Th2 responses evolve in humans, and potentially provide insight into therapeutic interventions.
Author Milner, Joshua D.
AuthorAffiliation Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH) , Bethesda, MD , United States
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Keywords T-cell receptor repertoire
monogenic syndromes
atopic disease
primary immunodeficiencies
signaling pathways
Language English
License This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
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Specialty section: This article was submitted to T Cell Biology, a section of the journal Frontiers in Immunology
Reviewed by: António Gil Castro, University of Minho, Portugal; Lawrence Kane, University of Pittsburgh, United States
Edited by: Wanjun Chen, National Institutes of Health (NIH), United States
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Snippet Stimulation of naïve CD4 T cells with weak T cell receptor agonists even in the absence of T helper-skewing cytokines can result in IL-4 production which can...
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SubjectTerms Actins - metabolism
atopic disease
Biomarkers
Cells, Cultured
Coculture Techniques
Cytoskeleton - metabolism
Dendritic Cells - immunology
Dendritic Cells - metabolism
Humans
Hypersensitivity, Immediate - genetics
Hypersensitivity, Immediate - immunology
Hypersensitivity, Immediate - metabolism
Immunology
Leukocytes, Mononuclear - immunology
Leukocytes, Mononuclear - metabolism
Lymphocyte Activation - genetics
Lymphocyte Activation - immunology
monogenic syndromes
Mutation
Phenotype
primary immunodeficiencies
Receptors, Antigen, T-Cell - genetics
Receptors, Antigen, T-Cell - metabolism
Signal Transduction
signaling pathways
T-cell receptor repertoire
Th2 Cells - immunology
Th2 Cells - metabolism
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Title TCR Signaling Abnormalities in Human Th2-Associated Atopic Disease
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