Jason Scott Knight MD, PhD

Assistant Professor, Internal Medicine
Specialties: 
Rheumatology, Internal Medicine

Locations

U of M Rheumatology

Taubman Center Floor 3 Reception A
1500 E Medical Center Dr SPC 5370
Ann Arbor
MI
48109
Phone:
734-647-5900
Fax:
734-615-5308

Credentials

Medical School or Training

  • University of Michigan Medical School, 2007

Residency

  • University of Michigan Health System, Internal Medicine, MI, 2010

Fellowship

  • Internal Medicine Rheumatology, University of Michigan Health System, 2012

Board Certification

  • Internal Medicine

  • Rheumatology

Research

My laboratory is interested in the mechanisms by which exaggerated immune responses lead to vascular damage and thrombosis in the rheumatic diseases.  In particular, we study systemic lupus erythematosus (SLE) and the antiphospholipid antibody syndrome (APS), using both human and murine systems to understand how neutrophils and platelets become abnormally activated in these diseases.  Recent publications have focused on the role of neutrophil extracellular traps (NETs) in murine SLE, while we are currently recruiting human subjects for basic research into these pathways in APS.  

Biography

Dr. Knight received his M.D. and Ph.D. degrees from the University of Michigan, and completed the majority of his molecular biology Ph.D. research in the lab of Dr. Erle Robertson at the University of Pennsylvania.  His fellowship in rheumatology was at the University of Michigan, where he pursued postdoctoral research in the lab of Dr. Mariana Kaplan.  During fellowship, he received the prestigious American College of Rheumatology Distinguished Fellow Award, as well as a Rheumatology Research Foundation Scientist Development Award.  He joined the faculty in 2012, and was promoted to Assistant Professor in 2014.  Dr. Knight’s research focuses on abnormal innate immune responses in systemic lupus erythematosus (SLE) and the related antiphospholipid antibody syndrome (APS).  His lab is especially interested in the role of neutrophils and platelets in the vascular damage and thrombosis inherent to these diseases.

Links