Heath Lab Personnel
- About the Heath group
- The Heath laboratory works in close collaboration with the Carbone Laboratory.
The Heath Lab is broadly interested in the role and function of CD8 killer T cells. CD8 killer T cells are critical for protection against viral infection and tumour development however when inappropriately activated they will attack the body’s own tissues leading to autoimmune disease. The lab uses novel models and cellular immunology tools to understand and dissect CD8 killer T cell function. An exciting new aspect to the research repertoire is the ability to directly visualise cellular interactions with 2-photon microscopy. Current research is examining cytotoxic T cell function in a number of different aspects as described below in major research projects.
- Imaging the priming of CD8 killer T cell responses to Herpes Simplex Virus-1 skin infection
- Imaging effector and memory T cell responses in the skin following Herpes Simplex Virus-1 infection
- Analysis of lymphoid stromal cells in the steady-state and during infection
- Understanding how dendritic cells shape virus-specific T cell responses
- T-cell-dendritic cell interactions in secondary immune responses to Herpes Simplex Virus
- CD8 killer T cell tolerance to self antigens
- Search for inhibitors of cross-presentation in dendritic cells
- Improved vaccines by targeting to dendritic cells
- Investigation of CD8 killer T cells in malaria
- Analysis of antigen presentation during malaria infection
About the Heath group
Dr Gayle Davey (SRO) | Please also see Gayle Davey's home page
Dr Scott Mueller (SRO) | Please also see Scott Mueller's home page
Dr Catherine van Vliet (RO)
Dr Daniel Fernandez Ruiz (RO)
Dr Ali Zaid (RO)
Dr Julia Gregory (RO)
Lei Shong Lau (PhD Student)
Brooke Davies (Research Assistant)
JoAnn Kellan (Research Assistant)
Amanda Turner (Research Assistant)
Biba Horvatic (Research Assistant)
Dr Ann Cornish (Research Administration Officer)
- Bedoui S, Prato S, Mintern J, Gebhardt T, Zhan Y, Lew AM, Heath WR, Villadangos JA, Segura E.
Characterization of an immediate splenic precursor of CD8+ dendritic cells capable of inducing antiviral T cell responses.
J Immunol 2009; 182: 4200-7.
- Bedoui S, Whitney PG, Waithman J, Eidsmo L, Wakim L, Caminschi I, Allan RS, Wojtasiak M, Shortman K, Carbone FR, Brooks AG, Heath WR.
Cross-presentation of viral and self antigens by skin-derived CD103+ dendritic cells.
Nat Immunol 2009; 10: 488-95.
These papers defined the function of a new dendritic cell subset termed CD103+ dendritic cells. They showed that CD103+ dendritic cells cross-present skin antigens and prime CD8 killer T cells during viral infection.
- Belz GT, Smith CM, Kleinert L, Reading P, Brooks A, Shortman K, Carbone FR, Heath WR.
Distinct migrating and non-migrating dendritic cell populations are involved in MHC class I-restricted antigen presentation after lung infection with virus.
Proc Natl Acad Sci USA 2004; 101: 8670-75. (IF= 9.64. 21)
This study was the first to provide evidence for antigen transfer from migratory dendritic cells to resident dendritic cells for induction of immunity to infection.
- Allan RS, Smith CM, Belz GT, van Lint AL, Wakim LM, Heath WR, Carbone FR.
CTL immunity after epidermal infection involves CD8 dendritic cells, but not Langerhans cells.
Science 2003; 301: 1925-8.
This paper presented results which shifted the paradigm that Langerhans cells (LC) stimulate responses from the skin by showing that they did not stimulate CD8 killer T cell immunity to Herpes Simplex Virus infection of the skin.
- Bennett SRM, Carbone FR, Karamalis F, Flavell RA, Miller JFAP, Heath WR.
Help for cyotoxic T cell responses is mediated via CD40 signalling.
Nature 1998; 393: 478-480.
This is an extremely highly cited paper (in 2011 over 1200 citations) in a world leading scientific journal showing that CD4 helper T cells help CD8 killer T cells by licensing dendritic cells through CD40L signalling of CD40.
- Kurts C, Kosaka H, Carbone FR, Miller JFAP, Heath WR.
Class I-restricted cross-presentation of exogenous self antigens leads to deletion of autoreactive CD8+ T cells.
J Exp Med 1997; 186: 239-245.
This study showed self antigens from tissues (for example, the pancreas) can be cross-presented in the steady-state and that this leads to deletion of self-reactive T cells to maintain tolerance and to reduce the potential for autoimmunity.