Regulation of IL-1beta in inflammation

Regulation of IL-1beta in inflammation

Project details

Interleukin-1β (IL-1β) is a cytokine that causes inflammation to protect against infections. However, IL-1β can also promote autoinflammatory diseases such as multiple sclerosis, diabetes and hereditary cryopyrin-associated periodic syndromes.

Despite its clear relevance to human health, we still do not understand how IL-1β is released from cells. Unlike nearly all secreted cytokines, IL-1β does not contain a conventional secretory sequence. Reports have suggested that IL-1β is released as a consequence of cell death, but we have recently published conclusive evidence that IL-1β secretion occurs by an active mechanism that does not require membrane rupture (Conos, Cell Death & Differentiation 2016). 

The aim of this project will be to use molecular biology and proteomic techniques to determine how IL-1β is secreted to trigger innate immunity.

About our research group

We have a specific interest in utilising advanced proteomic techniques to answer biological questions.  These overlap with our expertise in studying how inflammasome protein complexes can trigger IL-1β activation and secretion (e.g. Allam et al., EMBO Reports 2104: Lawlor et al., Nature Comm. 2015: Conos et al., CDD 2016). This project will therefore utilise these two strengths to identify the mechanism of IL-1β secretion which, despite intensive efforts, has eluded researchers for decades.

 

Researchers:

Dr James Vince

Dr James Vince in a laboratory
Dr
James
Vince
Laboratory Head
Dr Lisa Lindqvist
Dr
Lisa
Lindqvist
Cell Signalling and Cell Death division
Dr Jarrod Sandow profile shot
Dr
Jarrod
Sandow
Systems Biology and Personalised Medicine division

Project Type: