Apoptosis amongst specific and bystander T cells in chronic bacterial infection [ 2001 - 2003 ]

Research Grant

Researchers: Christina Cheers (Principal investigator)

Brief description When an infection occurs the immune cells (lymphocytes) proliferate in order to initiate and expand the immune response. If the body had no mechanisms to limit proliferation, the numbers of cells would soon overwhelm the body. Working with simple protein antigens rather than infection, other workers have found that once T lymphocytes have been activated and the immune response triggered, they soon undergo a process of self destruction called apoptosis. However, during infection, if the limits to lymphocyte proliferation are imposed before the infecting bacterium is eliminated, full expression of immunity does not occur and chronic infection may result. We believe that this contributes to the chronicity of such infections as tuberculosis and leprosy. We also suspect that, during infection, not only protective T lymphocytes proliferate, but also nonspecific bystander cells. This exaggerates the problem of lymphocyte proliferation and adds to immunopathology (immune damage). We have established an animal model of chronic bacterial infection in order to study how apoptosis is induced in T lymphocytes and how its adverse effects may be overcome. We hypothesize that apoptosis may be induced by one or more of a number of mechanisms, and that they may differ for the specific protective cells and the bystander cells. Once we understand the mechanisms apoptosis of specific lymphocytes may be prevented without harming the body. This has the potential to open new areas of immunotherapy (manipulating the immune response) of these diseases.

Funding Amount $AUD 317,545.90

Funding Scheme NHMRC Project Grants

Notes Standard Project Grant