Amplifying IFN-γ Signaling in Dendritic Cells by CD11c-Specific Loss of SOCS1 Increases Innate Immunity to Infection while Decreasing Adaptive Immunity.
Publication Title
Journal of immunology (Baltimore, Md. : 1950)
Document Type
Article
Publication Date
1-1-2018
Keywords
Adaptive Immunity; Animals; Bacterial Vaccines; CD11c Antigen; CD8-Positive T-Lymphocytes; Cells, Cultured; Cytotoxicity, Immunologic; Dendritic Cells; Humans; Immunity, Innate; Interferon-gamma; Killer Cells, Natural; Listeria monocytogenes; Listeriosis; Mice; Mice, Inbred C57BL; Mice, Knockout; Suppressor of Cytokine Signaling 1 Protein
Abstract
Although prophylactic vaccines provide protective humoral immunity against infectious agents, vaccines that elicit potent CD8 T cell responses are valuable tools to shape and drive cellular immunity against cancer and intracellular infection. In particular, IFN-γ-polarized cytotoxic CD8 T cell immunity is considered optimal for protective immunity against intracellular Ags. Suppressor of cytokine signaling (SOCS)1 is a cross-functional negative regulator of TLR and cytokine receptor signaling via degradation of the receptor-signaling complex. We hypothesized that loss of SOCS1 in dendritic cells (DCs) would improve T cell responses by accentuating IFN-γ-directed immune responses. We tested this hypothesis using a recombinant
Area of Special Interest
Cancer
Specialty/Research Institute
Oncology
Specialty/Research Institute
Earle A. Chiles Research Institute
