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VERSION:2.0
CALSCALE:GREGORIAN
METHOD:PUBLISH
BEGIN:VEVENT
DTSTAMP:20160706T152407Z
DTSTART:20160711T143000Z
DTEND:20160711T153000Z
SUMMARY:MCCIR AZ/GSK Update Seminar 
UID:{http://www.columbasystems.com/customers/uom/gpp/eventid/}ids-iqb1bp3
 g-84yf8n
DESCRIPTION:Identifying immunological biomarkers to predict treatment res
 ponse in rheumatoid arthritis\nBen Mulhearn\nRheumatoid arthritis (RA) i
 s the most common autoimmune disease\, affecting 5 – 10 in 1000 people. 
 If left untreated RA can cause permanent joint damage and chronic disabi
 lity. Good evidence shows that treating inflammation early leads to less
  irreversible damage and improves patient outcomes. Many patients will e
 nd up on a biologic drug having failed a 6-month trial of conventional d
 rugs. Even so\, not all patients will respond to their first biologic dr
 ug and there is currently no way to predict which drug will work first i
 n each individual patient.\nMy aim is to develop an immunological assay 
 that will help to predict which type of biologic drug will be effective 
 in treating each individual patient with RA\, prior to starting treatmen
 t. This will be achieved by stimulating peripheral blood mononuclear cel
 ls taken from patients who are about to start a biologic drug\, immunoph
 enotyping subjects\, and using a multivariate statistical regression fra
 mework to correlate immune phenotypes with clinical response data collec
 ted at 3 and 6 months. An assay with this power would be a major leap fo
 rward for precision medicine in rheumatoid arthritis\, and has the poten
 tial to apply to other autoimmune diseases treated with biologic drugs.\
 n\nExploiting the immune system in the treatment of cancer\nDr Amy Adlar
 d\nInvariant NKT cells are activated by cytokines or ligation of their i
 nvariant T cell receptor with glycolipid antigens\, resulting in direct 
 cytotoxicity and/or the production of Th1/Th2 cytokines. The ligand ?Gal
 Cer has shown limited efficacy as a cancer monotherapy in vivo\, and req
 uired additional IL12 for optimal effect. We have tested a new Th1-skewi
 ng ?GalCer analogue\, 7DW8-5\, in both transgenic and implanted mouse mo
 dels of melanoma. Fortnightly dosing with the ligand delayed tumour grow
 th in both models\, and resulted in activation of various immune cells i
 n vivo. \nI am also interested in the role of the lung microenvironment 
 and promotion of tumour metastasis. Alveolar macrophages (AM) have major
  roles in resolution of lung inflammation and prevention of injury follo
 wing viral infection\, where they have been shown to increase expression
  of regulatory receptors long-term after resolution\; however little is 
 known regarding their role in metastatic disease. AM have recently been 
 shown to be conducive of breast cancer metastasis in vivo\, however\, th
 e mechanisms underlying this effect are largely unknown. I have begun to
  profile AM following s.c. implantation of tumour cells at a distant sit
 e\, with the aim of revealing targets that could be manipulated to alter
  the innate activation threshold and reduce lung metastasis. Future stud
 ies will determine whether various tissue-specific immune landscapes fol
 lowing infection are more conducive or inhibitory to metastasis.\n\n
STATUS:TENTATIVE
TRANSP:TRANSPARENT
CLASS:PUBLIC
LOCATION:Michael Smith Lecture Theatre\, Michael Smith Building\, Manches
 ter
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