Associate Professor Jinhua Lu - National University of Singapore

Associate Professor Jinhua Lu - National University of Singapore

Davis Auditorium
Start Time: 
Tue, 24/05/2022 - 4:00pm
End Time: 
Tue, 24/05/2022 - 5:00pm

WEHI Special MINTI Seminar hosted by Ken Shortman & Michael Chopin

Associate Professor Jinhua Lu

Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University of Singapore


The origin of nuclear autoimmunity: nucleolin as an autoantibody target and a potential alarmin trigger


Davis Auditorium

Online access via Slido and enter code #WEHIimmunology

Including Q&A session


Monthly International Immunology Seminar Series (MINTI)

Systemic lupus erythematosus (SLE) is an autoimmune disease caused by immune complexes of autoantibodies and nuclear antigens. What causes nuclear antigens to trigger autoantibodies remains elusive. Most SLE patients lack defined genetic contributions but monogenic SLE does occur in complement C1 (C1qC1r2C1s2) deficiency. After my sabbatical in WEHI (2010), we began to delineate the C1 pathway in limiting nuclear autoimmunogenecity. We first identified dominant C1q binding to necrotic cell nucleoli which are abundant with autoantigens and then discovered nucleolin, which is an abundant nucleolar autoantigen, was a potent alarmin. The alarmin activity was mapped to its 48-amino acid GAR/RGG motif. Two more nucleolar alarmins, i.e. fibrillarin and GAR1, were predicted and validated based on the GAR/RGG motif. We think that nucleolin triggers nuclear autoimmunity by inducing its own autoantibodies. The GAR/RGG motif is also being used to develop vaccines.

Jinhua Lu completed undergraduate studies (Animal Husbandry, Hebei Agricultural University, 1981-5) and M.Sc. training (Molecular Engineering, Beijing Agricultural University, 1985-8) in China. He obtained his PhD in Immunochemistry and his initial postdoctoral training at the University of Oxford (1988-94). He moved to the National University of Singapore in 1994 as a Lee Kuan Yew Research Fellow and he is now an Associate Professor in its Department of Microbiology and Immunology. His lab studies the role of complement C1 and dendritic cells in the causes of nuclear autoimmunity. They have recently also embarked on the development/delivery of cancer vaccines, taking advantage of expertise in dendritic cells and the GAR/RGG motif.


All welcome!