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 in | Frontiers in immunology Vol. 9; p. 719 |
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Format | Journal Article |
Language | English |
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Frontiers Media S.A
16.04.2018
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ISSN | 1664-3224 1664-3224 |
DOI | 10.3389/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. |
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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 |
AuthorAffiliation_xml | – name: Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH) , Bethesda, MD , United States |
Author_xml | – sequence: 1 givenname: Joshua D. surname: Milner fullname: Milner, Joshua D. |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29713322$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1016_j_coi_2019_06_002 crossref_primary_10_3389_fimmu_2018_02078 crossref_primary_10_3389_fimmu_2018_02148 crossref_primary_10_1097_MD_0000000000036892 crossref_primary_10_1126_sciimmunol_abn3800 crossref_primary_10_1097_ACI_0000000000000481 |
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Keywords | T-cell receptor repertoire monogenic syndromes atopic disease primary immunodeficiencies signaling pathways |
Language | English |
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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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