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Jason Waithman

Researcher at University of Western Australia

Publications -  55
Citations -  4998

Jason Waithman is an academic researcher from University of Western Australia. The author has contributed to research in topics: CD8 & Cytotoxic T cell. The author has an hindex of 25, co-authored 51 publications receiving 4409 citations. Previous affiliations of Jason Waithman include Ludwig Institute for Cancer Research & Walter and Eliza Hall Institute of Medical Research.

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Migratory dendritic cells transfer antigen to a lymph node-resident dendritic cell population for efficient CTL priming.

TL;DR: After skin infection with herpes simplex virus, cytotoxic T lymphocyte activation required MHC class I-restricted presentation by nonmigratory CD8(+) DCs rather than skin-derived DCs, which supports the argument for initial transport of antigen by migratingDCs, followed by its transfer to the lymphoid-resident DCs for presentation and CTL priming.
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Cross-presentation of viral and self antigens by skin-derived CD103 + dendritic cells

TL;DR: It is shown that CD103+ DCs were the migratory subset most efficient at processing viral antigens into the major histocompatibility complex class I pathway, potentially through cross-presentation.
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The Dendritic Cell Populations of Mouse Lymph Nodes

TL;DR: The putative LC-derived DC among skin emigrants and in LN also showed strong intracellular staining of langerin, and was identified as the mature form of epidermal Langerhans cells (LC).
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Dendritic cell-induced memory T cell activation in nonlymphoid tissues.

TL;DR: Results revealed that memory CD8+ T cell responses can be initiated within peripheral tissues through a tripartite interaction that includes CD4+ T cells and recruited dendritic cells, lending evidence for the existence of a sophisticated T cell response mechanism in extra-lymphoid tissues that can act to control localized infection.
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Cognate CD4+ T cell licensing of dendritic cells in CD8+ T cell immunity

TL;DR: It is shown here that help is essential for the generation of CTL immunity to herpes simplex virus 1 and that CD4+ T cells mediate help in a cognate, antigen-specific way and that C TL immunity may be heavily dependent on cognate DC licensing.