Our lupus research

Our lupus research

Lupus research team at Garvan

L-R: Dr Joanne Reed, Prof Chris Goodnow, Dr Daniel Suan, Prof Robert Brink

Our lupus research hopes to identify and isolate the immune cells responsible for making self-attacking autoantibodies. We want to know how they’re different from normal immune cells.

Establishing these differences will show how they develop, and what causes them to switch to attack the body. This will lead to new treatments, for e.g. by revealing cellular vulnerabilities that respond to targeted drug therapies. The ultimate aim is to eliminate the bad (self-attacking) cells while preserving the rest of the immune system. 

Our research uses cellular genomics to study these individual cells, and understand how and why they’ve ‘gone rogue’. The mutations or variations in the DNA of these cells may point to the common root cause of all autoimmune disease.

Our focus is also targeted at lupus nephritis: a common and devastating symptom of lupus where autoantibodies attack the kidneys.

Key areas of investigation

Prof Chris Goodnow
Prof Chris Goodnow

Hope Research – finding the cause of autoimmune disease

Garvan’s Professor Chris Goodnow believes there may be a common cause underlying all autoimmune diseases. These are the ‘rogue’ immune cells causing tissue and organ damage as the body attacks itself.

We want to fix the underlying cause of autoimmune diseases like lupus.

Most of the current treatments for lupus are directed at the immune system itself: suppressing the whole immune system with steroids and other drugs, because we can’t identify and eradicate the cells that have gone rogue.

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Prof Robert Brink
Prof Robert Brink

Antibodies and the germinal centre

We’re working out why a small proportion of people (less than 10%) make the autoantibodies that cause diseases like lupus; and others do not.  The current focus is on a particular structure in lymph glands and the spleen called the ‘germinal centre’.

The white blood cells destined to make antibodies (B lymphocytes) collect there and mature into cells which produce antibodies to foreign microorganisms. This is the normal immune response. According to our recent work, it seems the maturation process in germinal centres is defective in autoimmune diseases, resulting in the escape of autoantibody-producing  B lymphocytes and a breakdown in immune tolerance. 

The next step will be to devise therapeutic strategies for reprogramming the germinal centre to shut down autoimmunity.

National and international collaborations

  • New York University School of Medicine
  • UNSW Sydney
  • Flinders University.