Rheumatic fever (RF) is one of New Zealand’s starkest examples of health inequity, with Māori and Pacific children 20-40 times more likely than all other New Zealand children to develop the disease. RF is triggered by Streptococcus A (StrepA) infections and can develop into chronic rheumatic heart disease (RHD). There is currently a complete lack of treatment options available to RF patients to halt cardiac damage and progression to RHD. Improved understanding of RF disease mechanisms is urgently needed to determine pathways that could be targeted by existing drugs to reduce progression. We observed a marked elevation of a particular antibody type (subclass IgG3) in RF patients and will use advanced laboratory methods to map the immune mechanisms associated with this increase. This will identify intervention pathways that may be interrupted by immune modulating drugs already in clinical use for other diseases with the potential to stop RF patients developing chronic RHD.