Please wait while the transcript is being prepared...
Hello everybody. I'm Anne Cooke.
I'm the Emeritus Professor of Immunobiology in
the Pathology Department in the University of Cambridge.
Today I'm going to talk about immune tolerance and autoimmunity.
Now, the aim of this lecture is really to understand
how self-tolerance is established and maintained,
and how it might be broken, and obviously,
if it's broken, it has the possibility of leading to autoimmune diseases.
Now, a very simplistic view of an immune response is that antigen enters the system,
is taken up and presented by a dendritic cell and
presented to a helper T-cell in the context of MHC class II.
The helper T-cell can provide help for a cytotoxic T-cell or to a B-cell,
and the B-cell can elaborate antibodies.
It also has been activated by antigen as a cytotoxic T-cell.
Now, once the antigen is clear from the immune system,
then everything returns back to baseline to homeostasis,
and the immune response itself dies down, but of course,
you will have some memory responses almost certainly generated during that time.
The type of T-cell that a naive T-cell differentiates into
is dependent on the cytokines that are around at the time of the initial stimulation.
For example, in the context of IL-12 being produced by dendritic cells,
you will get a predominantly Th1 response.
That response is very effective at dealing with viruses and bacteria,
and is important for intracellular immunity in the context of how far you get Th2 cells,
and Th2 cells can help B-cells and they're really important
in dealing with extracellular large pathogens, for example, helminths.
IL-6 together with TGF-beta is involved in
the generation of Th17 cells which are important to mucosal immunity
and TGF-beta alone in the absence of inflammatory cytokines can
lead to the development in the periphery of regulatory T-cells which are host protective.