Deficiency in IL-17-committed Vγ4(+) γδ T cells in a spontaneous Sox13-mutant CD45.1(+) congenic mouse substrain provides protection from dermatitis
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Immature B Cell Egress from Bone Marrow Is SOCS3 IndependentIL-21R signaling suppresses IL-17+ gamma delta T cell responses and production of IL-17 related cytokines in the lung at steady state and after Influenza A virus infection.IL-17-producing γδ T cells switch migratory patterns between resting and activated states.In vivo photolabeling of tumor-infiltrating cells reveals highly regulated egress of T-cell subsets from tumors.Differential developmental requirement and peripheral regulation for dermal Vγ4 and Vγ6T17 cells in health and inflammation.Interleukin 17-producing γδT cells promote hepatic regeneration in mice.Nociceptive sensory neurons drive interleukin-23-mediated psoriasiform skin inflammation.γδT cells are prevalent in the proximal aorta and drive nascent atherosclerotic lesion progression and neutrophilia in hypercholesterolemic mice.IL-17A gene transfer induces bone loss and epidermal hyperplasia associated with psoriatic arthritis.Global characterization of differential gene expression profiles in mouse Vγ1+ and Vγ4+ γδ T cells.The TCR ligand-inducible expression of CD73 marks γδ lineage commitment and a metastable intermediate in effector specificationMixing Signals: Molecular Turn Ons and Turn Offs for Innate γδ T-Cells.A Highly Focused Antigen Receptor Repertoire Characterizes γδ T Cells That are Poised to Make IL-17 Rapidly in Naive AnimalsThe thymic cortical epithelium determines the TCR repertoire of IL-17-producing γδT cells.Chronic ethanol feeding induces subset loss and hyporesponsiveness in skin T cellsGPR18 Controls Reconstitution of Mouse Small Intestine Intraepithelial Lymphocytes following Bone Marrow Transplantation.Dermal γδ T cells--What have we learned?Cutting Edge: PD-1 Regulates Imiquimod-Induced Psoriasiform Dermatitis through Inhibition of IL-17A Expression by Innate γδ-Low T Cells.Inflammation induces dermal Vγ4+ γδT17 memory-like cells that travel to distant skin and accelerate secondary IL-17-driven responses.IL-15 receptor α signaling constrains the development of IL-17-producing γδ T cells.Nociceptive Sensory Fibers Drive Interleukin-23 Production from CD301b+ Dermal Dendritic Cells and Drive Protective Cutaneous ImmunityDermal γδ T Cells Do Not Freely Re-Circulate Out of Skin and Produce IL-17 to Promote Neutrophil Infiltration during Primary Contact HypersensitivityTranscription factor networks directing the development, function, and evolution of innate lymphoid effectorsγδT17 cells promote the accumulation and expansion of myeloid-derived suppressor cells in human colorectal cancer.The NFκB-inducing kinase is essential for the developmental programming of skin-resident and IL-17-producing γδ T cells.Calcitonin Gene-Related Peptide-Exposed Endothelial Cells Bias Antigen Presentation to CD4+ T Cells toward a Th17 Response.Skin Immunity to Candida albicans.IL-17A-producing resident memory γδ T cells orchestrate the innate immune response to secondary oral Listeria monocytogenes infectionMigratory and adhesive cues controlling innate-like lymphocyte surveillance of the pathogen-exposed surface of the lymph node.Functional development of γδ T cells.The skin-resident and migratory immune system in steady state and memory: innate lymphocytes, dendritic cells and T cells.Molecular Mechanisms of Differentiation of Murine Pro-Inflammatory γδ T Cell Subsets.The Jekyll and Hyde story of IL17-Producing γδT Cells.IL-1β and IL-23 Promote Extrathymic Commitment of CD27(+)CD122(-) γδ T Cells to γδT17 CellsIL-2 Shapes the Survival and Plasticity of IL-17-Producing γδ T Cells.IL-1 receptor antagonist-deficient mice develop autoimmune arthritis due to intrinsic activation of IL-17-producing CCR2(+)Vγ6(+)γδ T cellsIL-17+ γδ T cells as kick-starters of inflammation.The majority of murine γδ T cells at the maternal-fetal interface in pregnancy produce IL-17.Effector γδ T Cell Differentiation Relies on Master but Not Auxiliary Th Cell Transcription Factors.Small molecule mediated inhibition of RORγ-dependent gene expression and autoimmune disease pathology in vivo.
P2860
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P2860
Deficiency in IL-17-committed Vγ4(+) γδ T cells in a spontaneous Sox13-mutant CD45.1(+) congenic mouse substrain provides protection from dermatitis
description
2013 nî lūn-bûn
@nan
2013年の論文
@ja
2013年論文
@yue
2013年論文
@zh-hant
2013年論文
@zh-hk
2013年論文
@zh-mo
2013年論文
@zh-tw
2013年论文
@wuu
2013年论文
@zh
2013年论文
@zh-cn
name
Deficiency in IL-17-committed ...... des protection from dermatitis
@en
type
label
Deficiency in IL-17-committed ...... des protection from dermatitis
@en
prefLabel
Deficiency in IL-17-committed ...... des protection from dermatitis
@en
P2093
P2860
P356
P1433
P1476
Deficiency in IL-17-committed ...... des protection from dermatitis
@en
P2093
Elizabeth E Gray
Francisco Ramírez-Valle
Jason G Cyster
Klaus E Karjalainen
P2860
P304
P356
10.1038/NI.2585
P407
P577
2013-04-28T00:00:00Z