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SUMMARY:&quot\;Chronic Inflammatory Diseases and Tryptophan Catabolism&quo
 t\;  - Prof. Andrew Mellor\; Professor of Translational Immunology\, Insti
 tute of Cellular Medicine\, University of Newcastle 
DTSTART:20180226T130000Z
DTEND:20180226T140000Z
UID:TALK96400@talks.cam.ac.uk
CONTACT:Bobbie Claxton
DESCRIPTION: \n \n\n\nChronic inflammation occurs in diseases that afflict
  many people\, including infections\, autoimmune diseases and cancer. Chro
 nic immune activation (CIA) is a hallmark of these diseases because unreso
 lved inflammation sustains immune cell activation. During CIA\, immune eff
 ector and regulatory processes counter-balance each other\, creating state
 s of inflammatory homeostasis in local lymphoid tissues. Over time\, CIA c
 auses progressive immune dysfunction\, pathology and worsening comorbiditi
 es including pain\, depression and fatigue. Rapid activation of Foxp3-line
 age 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 d
 riving early pro-inflammatory (immune stimulatory) responses during infect
 ions\, autoimmune syndromes and tumour growth. IFN-I also induces some APC
 s to express the enzyme indoleamine 2\,3 dioxygenase (IDO)\, which activat
 es Tregs and suppresses effector T cells by catabolizing the amino acid tr
 yptophan (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. C
 urrent research on factors that contribute to CIA during chronic disease a
 nd how CIA can be manipulated for therapeutic benefit will be discussed. 
LOCATION:Babraham - The Cambridge Building\; The Kings Hedges Room
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