Projects

Characterising the cause of human inflammation in autoimmune disease


Fc?R (the receptors for IgG) are important for pathogenesis in antibody-driven autoimmunity. Fc?RIIa is the most abundant and widespread human Fc-receptor.

We have shown that human Fc?RIIa expressed in appropriate cellular distributions at physiological levels in transgenic mice is sufficient to confer susceptibility to collagen-induced arthritis and spontaneous multi-system autoimmunity. We are currently investigating the molecular and cellular basis of Fc?RIIa-driven autoimmunity.

The presence of Fc?RIIa lowers the threshold of activation of innate immune cells by autoantibodies that drive the effector arm of pathogenic inflammation. We can completely inhibit the progress of this information by targeting FcgRIIa with either newly designed drugs or engineered monoclonal antibodies.

Our research shows that targeting this receptor at the right time can prevent the progress of the disease and that T cells secreting the proinflammatory cytokine IL-17 are elevated in Fc?RIIa-transgenic mice. We are now investigating if Fc?RIIa plays a role in skewing adaptive immunity.

Publications

2011

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1993

Contact Details

For any general enquiries relating to this project, please contact:

Professor Mark Hogarth

Head, Immune Therapies Group

Telephone

+61392822111

Email

mark.hogarth@burnet.edu.au