Lin Shen, MD, PhD

Assistant Professor

Autoimmune rheumatic diseases, which constitute a broad range of chronic illnesses, cause significant morbidity and mortality in the US and worldwide. T cell receptor (TCR) recognition and signaling have long be recognized to play a critical role in the pathogenesis of autoimmune diseases. However, how altered TCR signaling strength affects immune tolerance and promotes autoimmunity remains incompletely understood. Dr. Shen’s research seeks to understand how abnormal TCR signaling resulting from mutations from human patients with complex autoimmune syndrome may alter T cell antigen sensitivity, affect T helper cell fate, and impair immune tolerance. Studying human monogenic diseases with known genetic defects and autoimmune phenotypes provides us with a unique opportunity for advancing our knowledge of disease pathogenesis of more common polygenic autoimmune diseases. These studies may also have implications in preventing cancer immunotherapy related adverse events and identification of new therapeutic targets for autoimmune diseases.
Fellowship, 2017 - Rheumatology, University of California, San Francisco
Residency, 2014 - Internal Medicine, University of Pittsburgh Medical Center
PhD, 2010 - Pharmacology/Virology, Johns Hopkins University School of Medicine
MD, 2005 - , Peking Union Medical College
  1. ZAP-70 in Signaling, Biology, and Disease.
  2. A quantitative basis for antiretroviral therapy for HIV-1 infection.
  3. A critical subset model provides a conceptual basis for the high antiviral activity of major HIV drugs.
  4. Dose-response curve slope is a missing dimension in the analysis of HIV-1 drug resistance.
  5. Consistent inhibition of HIV-1 replication in CD4+ T cells by acyclovir without detection of human herpesviruses.
  6. Discovery of entry inhibitors for HIV-1 via a new de novo protein design framework.
  7. Unstimulated primary CD4+ T cells from HIV-1-positive elite suppressors are fully susceptible to HIV-1 entry and productive infection.
  8. Achieving a quantitative understanding of antiretroviral drug efficacy.
  9. A novel method for determining the inhibitory potential of anti-HIV drugs.
  10. New approaches for quantitating the inhibition of HIV-1 replication by antiviral drugs in vitro and in vivo.
  11. Isolation of a cellular factor that can reactivate latent HIV-1 without T cell activation.
  12. Preferential cytolysis of peripheral memory CD4+ T cells by in vitro X4-tropic human immunodeficiency virus type 1 infection before the completion of reverse transcription.
  13. Viral reservoirs, residual viremia, and the potential of highly active antiretroviral therapy to eradicate HIV infection.
  14. Dose-response curve slope sets class-specific limits on inhibitory potential of anti-HIV drugs.
  15. Decay dynamics of HIV-1 depend on the inhibited stages of the viral life cycle.
  16. The HBV drug entecavir - effects on HIV-1 replication and resistance.