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Notice of Seminar: Professor Arlene Sharpe (Harvard Medical School) on February 6 at 11 AM

Feb 06, 2025

We are pleased to announce a seminar by Professor Arlene Sharpe from Harvard Medical School.

Researchers in related fields, such as immunology and the tumor microenvironment, are encouraged to attend.

1. Date & Time:

Thursday, February 6, 2025
11:00 AM – 12:30 PM
(For those interested in having lunch with Professor Sharpe or meeting her separately afterward, please contact Professor Hyun-Sook Lee at hl212@snu.ac.kr.)

2. Venue:

Auditorium, 1st Floor, West Wing, Institute of Genetic Engineering

3. Speaker Introduction:

(See the attached file for details.)
Professor Sharpe’s discoveries were instrumental in the development of immune checkpoint blockade, which later led to the Nobel Prize.

  • Identified T cell co-stimulatory and co-inhibitory mechanisms
  • Her husband, Freedman, used CRISPR screening to discover immune checkpoints such as PD-1 and CTLA-4

4. Seminar Title & Abstract:

"Overcoming Resistance to PD-1 Checkpoint Blockade for Cancer Immunotherapy"

The PD-1 pathway delivers inhibitory signals that function as a brake for immune responses and has wide-ranging immunoregulatory functions. This pathway regulates the critical balance between stimulatory and inhibitory signals needed for effective immune responses to microbes and tumors, as well self-tolerance. The critical role of PD-1 in limiting anti-tumor immunity is demonstrated by the transformative effects of PD-1 cancer immunotherapy. Although PD-1 pathway inhibitors are revolutionizing cancer treatment, mechanistic insights are needed to understand why PD-1 pathway blockade works or fails in order to identify responders to PD-1 cancer immunotherapy and to develop rational combination therapies. This talk will discuss studies in mouse models that have identified mechanisms by which the PD-1 pathway regulates anti-tumor T cell responses, and gene perturbation approaches to discover new cancer immunotherapy targets and their mechanisms of action.