Breaking self-tolerance in lymphopenia:

Can we do it?

Supervisor:

Dr. Elena Shklovskaya

Senior Research Officer

T Cell Biology Group (group head, A/Prof B.Fazekas de St.Groth)

Centenary Institute of Cancer Medicine and Cell Biology

Email:   e.shklovskaya@centenary.usyd.edu.au

Phone    9565 6198

 

Project overview

 

What is self-tolerance and who is controlling it?

Put simply, self-tolerance is the inability of an organism to mount an immune response against self-antigens. A subpopulation of CD25+CD4+ T cells, termed regulatory T cells or Tregs, is responsible for preventing autoimmune diseases in animals and humans. “Treg” is a common term for several populations of regulatory T cells that differ in their ontogeny and perhaps mechanism(s) of suppression. Conditions that favour or hinder Treg functions are under the scrutiny of many research groups in the world.

 

The mouse model: some background facts

1) Mice double-transgenic for CD4 T cells expressing a given T cell receptor, and for model antigen that these T cell recognise (=self-antigen), do not develop autoimmune disease but instead have a large proportion of antigen-specific Tregs.

2) When CD4 T cells expressing a given T cell receptor are adoptively transferred into mice transgenic for the model antigen that these T cell recognise (=self-antigen), transferred T cells are deleted. No autoimmine disease develops.

3) Similar to (2), when CD4 T cells expressing a given T cell receptor are adoptively transferred into normal animals and then given a systemic antigen (e.g. large dose of oral or intravenous antigen), transferred T cells get deleted. No autoimmine disease develops.

4) When the same experiment (3) is performed in lymphopenic animals (irradiated of lacking T cells due to a genetic manipulation), deletion of adoptively transferred T cells in response to systemic antigen doesn’t occur. Animals can show signs of a transient autoimmine-like response, however they usually survive.

 

The goal of this project is to look at the mechanisms of T cell survival and “autoimmunity” in lymphopenic (rag-/-) mice that are either transgenic for model self-antigen (HEL:MCC) or receive a large “deletional” dose of model antigen (MCC). T cells expressing MCC-specific T cell receptor will be adoptively transferred into these rag-/- hosts, and the fate of transferred T cells, as well as animals’ health will be monitored. Specifically, we will concentrate on the conditions that favour the development of T cells with regulatory properties within the transferred T cell population.

 

List of techniques that will be used in conducting the research

Mouse in vivo techniques (including various ways of vaccination and intravenous injections, creating mouse chimeras, isolation of mouse lymph nodes and spleens, labelling of cell suspensions with CFSE dye and T cell adoptive transfer)

Nine-colour flow cytometryremember, we have the best Flow facility in Australia!

In vitro assays (T cell proliferation, cytokine re-stimulation)

Monoclonal antibody purification if required