"Chronic Inflammatory Diseases and Tryptophan Catabolism"

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• Prof. Andrew Mellor; Professor of Translational Immunology, Institute of Cellular Medicine, University of Newcastle
• Monday 26 February 2018, 13:00-14:00
• Babraham - The Cambridge Building; The Kings Hedges Room.

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Chronic inflammation occurs in diseases that afflict many people, including infections, autoimmune diseases and cancer. Chronic immune activation (CIA) is a hallmark of these diseases because unresolved inflammation sustains immune cell activation. During CIA , immune effector and regulatory processes counter-balance each other, creating states of inflammatory homeostasis in local lymphoid tissues. Over time, CIA causes progressive immune dysfunction, pathology and worsening comorbidities including pain, depression and fatigue. Rapid activation of Foxp3-lineage regulatory CD4 T cells (Tregs) by antigen presenting cells (APCs) is a key factor driving CIA . Interferon type I (IFN-I) is an innate response driving early pro-inflammatory (immune stimulatory) responses during infections, autoimmune syndromes and tumour growth. IFN -I also induces some APCs to express the enzyme indoleamine 2,3 dioxygenase (IDO), which activates Tregs and suppresses effector T cells by catabolizing the amino acid tryptophan (Trp). Thus, IFN -I is a pivotal response to inflammation, which drives CIA by co-activating immune stimulatory and regulatory processes. Some Trp catabolites made by IDO -expressing APCs are immune suppressive, while other Trp catabolites are neurotoxic and enhance pain sensitivity. Current research on factors that contribute to CIA during chronic disease and how CIA can be manipulated for therapeutic benefit will be discussed.

This talk is part of the Babraham Seminar series.

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