Supporting data for "The role of AIM2 inflammasome in Systemic Lupus Erythematosus"

Systemic Lupus Erythematosus is a chronic autoimmune condition in which the body mistakenly attacks itself. It’s aetiopathogenesis is highly complex. Increasing evidence suggests that the innate immune system is dysregulated in SLE. The inflammasomes mediate potent proinflammatory innate responses against invading pathogens and exogenous stressors via caspase-1-activation of IL-1beta and IL-18. In general, a cytosolic pattern recognition receptor (PRR), an ASC adaptor molecule, and procaspase-1 are required for the complete assembly of an inflammasome. Notably, elevated levels of IL-1beta and IL-18 have been noted in sera and tissues of SLE patients, highlighting their involvement in lupus development. The NLRP1, NLRP3, NLRC4 and AIM2 inflammasome are well-characterised inflammasomes in infection context. However, despite AIM2 (Absent in Melanoma 2) being a cytosolic dsDNA (SLE autoantigen) sensor, its role in human SLE remains unstudied. Hence, this project aimed to characterise the functional significance of AIM2 inflammasome in SLE patients. Briefly, the expression of the components of AIM2 inflammasome will be studied. Functional activity of the AIM2 inflammasome will also be analysed ex vivo. Mediators as well as the molecular mechanisms which contribute to the dysregulation of AIM2 inflammasome in SLE will be identified.