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02/21/2017 MoLife Research Seminar: Prof. Dr. Malgorzata Garstka

Tuesday, February 14, 2017 - 13:00
Lecture Hall of Research II

Invitation to a MoLife Research Seminar by:

Prof. Dr. Malgorzata (Gosia) Garstka, Professor in Molecular Immunology, Xi'an Jiaotong University, China


The molecular mechanism of antigen presentation by MHC class I molecules in health and auto-immune diabetes


Our immune system recognizes pathogenic antigens while staying tolerant towards selfantigens. Major histocompatibility complex (MHC) class I molecules present antigenic peptides at the plasma membrane for recognition by CD8+ T cells. There are multiple quality control steps to ensure proper antigen presentation.

First, MHC class I selects peptides. We demonstrated that MHC class I initially considers many, though not all, available peptides. The flexibility of the MHC I defines dissociation rates of peptides and thus selects against sub-optimal ones. Second, peptide selection is further optimized with the help of the MHC I-dedicated chaperone tapasin. Tapasin stabilizes MHC class I and accelerates peptide exchange until the optimal peptide is bound. Third, by stabilizing MHC class I, tapasin can also chaperone it out of the endoplasmic reticulum (ER).

Autoimmunity occurs when the immune system acts against oneself, that is, reacts to self-peptide MHC class I complexes. The observation of a genetic correlation between MHC class I polymorphism and Type I diabetes (T1D), as well as the auto-reactivity of CD8+ T cells toward pancreatic beta cells both suggest that MHC class I antigen presentation could directly contribute to autoimmunity in T1D I aim to understand how MHC class I antigen presentation leads to the development of T1D, create diagnostic tools to monitor disease occurrence and progression, define ways to interfere with T1D-associated antigen presentation.

Further information by: 

Prof. Dr. Sebastian Springer, Professor of Biochemistry and Cell Biology (Focus Area: Health - Life Sciences & Chemistry) Email:  s.springer [at] - Tel: +49 421 200-3243 - Link to Homepage: