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.



Dr James Vince

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

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