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My name is Hussein Al-Mossawi.
I'm a fellow and lecturer of medicine at St. Edmund Hall at the University of Oxford.
Today I'm going to be describing the immunology
underlying rheumatic inflammatory diseases.
The way I've structured this talk is to think about four key areas.
Firstly, the framework for the classification of immune-mediated rheumatic diseases.
Then secondly, we're going to focus on the interplay
between role of the genetics and environmental factors.
Thirdly, we'll consider some of
the key immune pathways that have been successfully targeted for therapeutic benefit,
and then we'll take a future perspective to look at technologies and
platforms coming through that will help inform us
and better our understanding of these diseases.
Now we're going to focus on the framework for
classifying immune-mediated rheumatic diseases.
Broadly speaking immune-mediated rheumatic diseases
can be thought of in three groups.
You have the biggest group and the best described rheumatic immune-mediated disease,
which is rheumatoid arthritis.
This is a destructive immune-mediated
inflammatory arthritis that affects predominantly the small joints of the hands.
It can affect multiple other systems in the body.
Some features of rheumatoid arthritis overlap with
autoimmune connective tissue diseases including systemic lupus erythematosus,
systemic sclerosis and inflammatory myopathies.
These diseases are multisystem in nature and can affect multiple organs.
They're characterised by specific autoantibody profiles that drive the pathology.
The connective tissue diseases can overlap with
rheumatoid arthritis and share this feature of autoantibody involvement.
In the red, you can see a group of
diseases that we call the seronegative spondyloarthropathies.
These diseases are not characterised by the presence of an autoantibody.
They include diseases such as ankylosing spondylitis,
psoriatic arthritis and enteropathic arthritis which is
associated with inflammatory bowel diseases such as Crohn's and ulcerative colitis.