Areas of Focus:

Adaptive ImmunityAnimal ModelsBiological & MechanisticExperimental Platforms & ModelsIn Vitro ModelsInnate ImmunityTherapeutic DevelopmentTranslational & ClinicalAllergic & Atopic DiseasesGastrointestinal Diseases
  • Associate Professor, Department of Laboratory Medicine, Yale School of Medicine, Yale University
  • Associate Professor, Department of Immunobiology, Yale School of Medicine, Yale University
  • Medical Director, Immune Monitoring Core Facility

Dr. Craig B. Wilen is an Associate Professor of Laboratory Medicine and Immunobiology at Yale School of Medicine, where he also serves as Medical Director of the Immune Monitoring Core Facility. He received his AB in Biology and Economics from Washington University in St. Louis and his MD and PhD from the University of Pennsylvania. He completed his residency in clinical pathology at Barnes-Jewish Hospital and his postdoctoral training at Washington University School of Medicine.

Dr. Wilen’s research focuses on host-pathogen interactions of RNA viruses, including coronaviruses and noroviruses. Among his most significant contributions, he discovered CD300lf as the first identified receptor for a norovirus and identified intestinal tuft cells as the physiologic target cell for mouse norovirus infection. Current work in his laboratory focuses on identifying mechanisms of viral entry, immunity, and pathogenesis for noroviruses, coronaviruses, and pre-emergent viruses with pandemic potential, with the goals of enabling improved risk stratification and developing better therapeutics and vaccines to reduce the disease burden from viral infections. For the Colton Consortium, his group is developing therapeutic bispecific antibodies for tuft cell-associated allergic disease.

Projects

Featured Pilot Projects

Development of Therapeutic Bispecific Antibodies for Tuft Cell Associated Allergic Disease
Project | Yale University

Development of Therapeutic Bispecific Antibodies for Tuft Cell Associated Allergic Disease

Developing T cell-redirecting bispecific antibodies to selectively eliminate tuft cells and break the cycle of Type 2 inflammation in CRSwNP.