Innate immune cells sense cellular ‘danger’ through a broad repertoire of innate immune receptors, such as Nod-like receptors and Toll-like receptors (TLRs). These signalling systems are interconnected through multiple layers of signal cross-talk. Our research aims to understand the mechanisms by which TLR and cytokine signalling pathways influence the assembly of inflammasomes and their downstream signalling pathways.

Projects:

• Mechanisms of inflammasome priming by TLRs
• Species specificity in inflammasome priming mechanisms

Select Publications:

1. Bezbradica JS¹, Coll R¹, Schroder K (2016).
   Sterile signals generate weaker and delayed macrophage NLRP3 inflammasome responses relative to microbial signals. Cellular & Molecular Immunology. In press. ¹Joint contribution.
    
2. Schroder K, Sagulenko V, Zamoshnikova A, Richards AA, Cridland JA, Irvine KM, Stacey KJ, & Sweet MJ (2012).
   Acute lipopolysaccharide priming boosts inflammasome activation independently of inflammasome sensor induction. Immunobiology 217(12):1325-1329. Pubmed
    
3. Schroder K, Irvine KM, Taylor MS, Bokil NJ, Le Cao KA, Masterman KA, Labzin LI, Semple CA, Kapetanovic R, Fairbairn L, Akalin A, Faulkner GJ, Baillie JK, Gongora M, Daub CO, Kawaji H, McLachlan GJ, Goldman N, Grimmond SM, Carninci P, Suzuki H, Hayashizaki Y, Lenhard B, Hume DA, & Sweet MJ (2012).
   Conservation and divergence in Toll-like receptor 4-regulated gene expression in primary human versus mouse macrophages. Proceedings of the National Academy of Science U S A 109(16):E944-953. Pubmed

Image: Artwork represents inflammasomes inside the cell and Toll-like Receptors on the cell membrane.