Speaker:

Ming-hui Zhao, Ph.D.

Renal Division, Peking University First Hospital

Peking-Tsinghua Center for Life Sciences, Beijing, PR. China

Abstract

Anti-GBM disease is a rare but severe glomerulonephritis. As a national referral nephrology center, we diagnosed over 500 patients with anti-GBM disease within 10 years. We recently identified natural anti-GBM antibodies from normal healthy individuals and potential mechanisms for their switching to pathogenic autoantibodies. By comparison of immune characteristics of serum anti-GBM antibodies in patients with different clinical phenotypes, we demonstrated IgG subclass switching, inter- and intra-epitope spreading of anti-GBM antibodies during disease progression. 

It has been hypothesized that anti-GBM disease might be initiated by microbial pathogens, by cross-reaction between microbial proteins and human α3(IV)NC1. We recently found a mutual T/B cell linear epitope on human on human α3(IV)NC1. Animal experiments demonstrated its antigenicity and pathogenicity and the critical amino acid motif of the epitope has been identified. Using the critical amino acid motif of the T/B cell epitope, we further identified a serial linear peptides derived from human accessible microbes using the NCBI protein Blast tool. Recombinant proteins from those possible microbial pathogens were produced to assess infection in patients with anti-GBM disease and to immunize disease susceptible rats to recapitulate human anti-GBM disease.

Time: 15:00-16:00 PM, Feb. 24th (Wednesday)

Venue: D326, Medical Science Building