|2015 Mackay group. L-R: Beatriz Garcillan, Aurelie Baldolli, Fabien Vincent, Ellen McAllister, Fabienne Mackay, Angela Nguyen, Pin Shie Quah, Rachel Lim, Florence Lim, Will Figgett|
Systemic lupus erythematosus (SLE), commonly known as lupus, is an autoimmune disease with no cure. Monash researchers have been working to understand the immunological causes of lupus in a mouse model so as to better understand the disease in humans. Such groundwork will enable the development of much more effective therapies for the treatment of lupus.
Professor Fabienne Mackay (former head of the Department of Immunology and Pathology), together with the department's Leukocyte Signalling laboratory headed by Associate Professor Margaret Hibbs have discovered that a certain type of innate B cell (immune cell), known as a B1b B cell, may be critical in the development of lupus.
Two types of mature B cells that are activated by toll-like receptor (TLR) signalling are B1 B cells and marginal zone (MZ) B cells. In the mouse model studied, these cells cause disease by infiltrating various tissues such as the salivary glands and kidneys. When the MZ and B1a B cells were removed from the mice, disease still occurred. When B1b B cells were removed also, mice were protected from all symptoms of lupus. Therefore B cells and CD19 signalling, specifically innate B cells, are very important in the development of lupus and may represent a target for treatment.
Reference: Fairfax KA, Tsantikos E, Figgett WA, Vincent FB, Quah P, LePage M, Hibbs ML, Mackay F. BAFF driven autoimmunity requires CD19 expression. J Autoimmun. 2015 Aug; 62: 1-10