Announcements

Seminar in KUTTAM, 19.10.2018, Muhammed Yüksel, PhD.

Author: Seminar in KUTTAM, 19.10.2018, Muhammed Yüksel, PhD.
Time: 12:00
Location: Koç University KUTTAM SNA 278

KUTTAM
 
SEMINAR IN KUTTAM

Friday, October 19th, 2018

 

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Speaker:  Muhammed Yüksel, PhD.
 

Institute of Liver Studies, King’s College London, Faculty of Life Sciences and Medicine, King’s College Hospital, London, UK

Title:        Prospects of autoimmune hepatitis/sclerosing cholangitis: rare diseases with ample research opportunities 

Time:      12:00 (Refreshments will be served at 11:45)

Place:      Koç University KUTTAM SNA 278
 
 

 

Prospects of autoimmune hepatitis/sclerosing cholangitis: rare diseases with ample research opportunities 
Childhood autoimmune liver disease is extremely rare and encompasses type-1 and type-2 autoimmune hepatitis (AIH) and autoimmune sclerosing cholangitis (ASC) both characterized by hepatocyte damage and in ASC also by cholangitis. Although the aetiology of both is unknown, AIH/ASC hallmarks include seropositivity for anti-nuclear and/or smooth muscle antibodies or anti-liver-kidney microsomal and/or anti-liver cytosolic type-1 antibodies. Additionally, elevated IgG, interface hepatitis, impaired immunoregulation by CD4posCD25highCD127negFOXP3pos T-cells (Tregs) are also seen alongside the presence of disease-predisposing genes such as human leukocyte antigens (HLA)-DR3/DR7/DR13. The currently available treatment is general immunosuppression, represented by steroids with or without azathioprine. However, up to 30% of the patients are poor/non-responders. Hitherto, we do not have any explanation as to why poor/non-response happens. Consequently, our research focuses on the very aspect of AIH/ASC patients being refractory to immunosuppression. Specifically, we aim to elucidate as to whether (i) particular HLAs, (ii) the immunological phenotype of Treg and (iii) cytokines (IL-2/IL-10) or (iv) other soluble factors (PD-1/CTLA-4) play a role in this phenomenon. Finally yet importantly, compelling evidence has emerged regarding the role of altered gut microbiota in AIH. Hence, we also (v) aim to investigate whether these changes in AIH are causal or not.