Inflammation and Cytokines Laboratory

The Jones laboratory investigates cytokine-regulated mechanisms that underpin chronic inflammation and immune-mediated tissue damage.

Vision

Inflammation is the body’s natural response to infection and tissue injury. Cytokines orchestrate all aspects of the inflammatory response including immune cell activation, migration, survival and effector function. Optimal control of this process ensures competent host defence. However, persistent or non-resolving episodes of inflammation often leads to tissue damage.

Our research examines how cytokines regulate the development, organisation, effector characteristics and maintenance of immune cells within inflamed tissues, with a particular interest in the negative regulation of inflammation to restore immune and tissue homeostasis.

With a primary focus in inflammatory arthritis, our research aims to exploit cytokines therapeutically and to define cytokine signatures that reflect patient outcomes.

Mission

Our ultimate goal is to aid clinical decision-making through identifying diagnostic markers and novel therapies that can inform patient stratification and treatment.

Approach

Spanning basic, pre-clinical and early clinical studies, we are investigating novel drugs for the treatment for inflammatory diseases and cytokine signatures that reflect disease activity. We combine cell culture, in vivo disease models, analysis of clinical samples and ‘big data’ approaches (e.g., RNA-sequencing), thus linking basic mechanistic studies with translational outcomes.

A particular area of focus is the mechanisms that govern the development, organisation and activity of lymph node-like compartments (called ectopic lymphoid structures; ELS) that develop within chronically inflamed tissues. Our research considers cross-disease and disease-specific mechanisms that regulate ELS across autoimmunity, infection and cancer. Here, we propose that immunomodulation of cytokine networks holds real potential for the treatment of chronic diseases where ELS feature.