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Start Over Descriptor "NK DC cross talk" Topic cd4-positive t-lymphocytes
2 results on '"NK DC cross talk"'

1. The Variable Genomic NK Cell Receptor Locus Is a Key Determinant of CD4+ T Cell Responses During Viral Infection.

Author

Raynor J, Lin A, Hummel SA, Lampe K, Jordan M, Hoebe K, and Hildeman DA

Subjects
Animals, Antigen Presentation genetics, Antigens, CD1d genetics, Dendritic Cells immunology, Interferon Type I biosynthesis, Killer Cells, Natural immunology, Lymph Nodes immunology, Lymphocyte Activation genetics, Lymphocytic Choriomeningitis virology, Mice, Mice, Inbred C57BL, Mice, Knockout, Pore Forming Cytotoxic Proteins deficiency, Pore Forming Cytotoxic Proteins genetics, CD4-Positive T-Lymphocytes immunology, Genetic Loci, Lymphocytic Choriomeningitis immunology, Lymphocytic choriomeningitis virus immunology, Receptors, Natural Killer Cell genetics
Abstract

Increasing evidence points to a key role for NK cells in controlling adaptive immune responses. In studies examining the role of CD1d on CD4+ T cell responses, we found that a line of CD1d-deficient mice on the C57BL/6J background had a homozygous 129 locus on chromosome 6 containing the entire NK cell gene cluster. Mice possessing this locus (C57BL/6.NKC 129 ) displayed a >10-fold reduction in antigen-specific CD4+ T cell responses after intracranial infection with lymphocytic choriomeningitis virus (LCMV). Neither parental strain displayed defects in viral-specific CD4+ T cell responses. Interestingly, following infection, increased numbers of NK cells accumulated in the lymph nodes of C57BL/6.NKC 129 mice and displayed enhanced in vivo functionality. Moreover, depletion of NK cells with anti-asialo-GM-1 antibody in C57BL/6.NKC 129 mice resulted in a >20-fold increase in viral-specific CD4+ T cell responses. Mechanistically, we found that dendritic cell antigen presentation and early type I IFN production were significantly decreased in C57BL/6.NKC 129 mice, but were restored in perforin-deficient C57BL/6.NKC 129 mice or following NK depletion. Together, these data reveal that the variable genomic regions containing the activating/inhibitory NK cell receptors are key determinants of antigen-specific CD4+ T cell responses, controlling type I IFN production and the antigen-presenting capacity of dendritic cells., (Copyright © 2020 Raynor, Lin, Hummel, Lampe, Jordan, Hoebe and Hildeman.)

Published
2020
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2. The Variable Genomic NK Cell Receptor Locus Is a Key Determinant of CD4+ T Cell Responses During Viral Infection

Author

Jana Raynor, Adora Lin, Sarah A. Hummel, Kristin Lampe, Michael Jordan, Kasper Hoebe, and David A. Hildeman

Subjects
0301 basic medicine, CD4-Positive T-Lymphocytes, Pore Forming Cytotoxic Proteins, lcsh:Immunologic diseases. Allergy, T cell, Antigen presentation, Cell, Immunology, CD4 T cells, NK cells, Lymphocytic Choriomeningitis, Lymphocyte Activation, 03 medical and health sciences, Mice, 0302 clinical medicine, Immune system, medicine, innate, Immunology and Allergy, Animals, Lymphocytic choriomeningitis virus, Original Research, Mice, Knockout, Antigen Presentation, NK DC cross talk, biology, Dendritic cell, Dendritic Cells, Acquired immune system, Molecular biology, adaptive immune response, 3. Good health, Killer Cells, Natural, Mice, Inbred C57BL, 030104 developmental biology, medicine.anatomical_structure, Genetic Loci, CD1D, Interferon Type I, biology.protein, Receptors, Natural Killer Cell, Lymph Nodes, viral infection, Antibody, Antigens, CD1d, lcsh:RC581-607, 030215 immunology
Abstract

Increasing evidence points to a key role for NK cells in controlling adaptive immune responses. In studies examining the role of CD1d on CD4+ T cell responses, we found that a line of CD1d-deficient mice on the C57BL/6J background had a homozygous 129 locus on chromosome 6 containing the entire NK cell gene cluster. Mice possessing this locus (C57BL/6.NKC129) displayed a >10-fold reduction in antigen-specific CD4+ T cell responses after intracranial infection with lymphocytic choriomeningitis virus (LCMV). Neither parental strain displayed defects in viral-specific CD4+ T cell responses. Interestingly, following infection, increased numbers of NK cells accumulated in the lymph nodes of C57BL/6.NKC129 mice and displayed enhanced in vivo functionality. Moreover, depletion of NK cells with anti-asialo-GM-1 antibody in C57BL/6.NKC129 mice resulted in a >20-fold increase in viral-specific CD4+ T cell responses. Mechanistically, we found that dendritic cell antigen presentation and early type I IFN production were significantly decreased in C57BL/6.NKC129 mice, but were restored in perforin-deficient C57BL/6.NKC129 mice or following NK depletion. Together, these data reveal that the variable genomic regions containing the activating/inhibitory NK cell receptors are key determinants of antigen-specific CD4+ T cell responses, controlling type I IFN production and the antigen-presenting capacity of dendritic cells.

Published
2020
Full Text
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