Jean-Laurent Casanova is pediatrician and immunologist by training, and has in practice become a human geneticist investigating the immunological basis of childhood infectious diseases. He has been recognized for his paradigm-shifting discoveries, demonstrating that life-threatening infectious diseases striking otherwise healthy children may be caused by single-gene inborn errors of immunity, including variations underlying mycobacterial diseases (IFN-y immunity), invasive pneumococcal disease (TIR), herpes simplex virus encephalitis (TLR3), and chronic mucocutaneous candidiasis (IL-17). Casanova was born in Paris, France, in 1963. He received his M.D. from the University of Paris Descartes in 1987, and his Ph.D. in immunology from the University of Paris Pierre and Marie Curie in 1992, after being trained at the Pasteur Institute in Paris and the Ludwig Institute for Cancer Research in Lausanne. Following a residency in pediatrics and a clinical fellowship in pediatric immunology-hematology, he was appointed a professor of pediatrics at the Necker Medical School in Paris. There, with Laurent Abel, he cofounded and codirected the Laboratory of Human Genetics of Infectious Diseases in 2001. He was appointed professor at Rockefeller in 2008 and named a Howard Hughes Medical Institute investigator in 2014. He is a member of both the National Academy of Sciences and the National Academy of Medicine.

Research Interests

Jean-Laurent Casanova/s laboratory studies the human genetic determinism of pediatric infectious diseases, particularly mycobacterial diseases, invasive pneumococcal disease, herpes simplex encephalitis, chronic mucocutaneous candidiasis, severe flu and Kaposi sarcoma. He is interested in identifying monogenic "holes" in the immune defense of otherwise healthy children who are susceptible to specific infectious diseases, work that has profound implications for and has resulted in a paradigm shift in clinical medicine and fundamental immunology. The lab aims to understand what it is that makes some children develop a severe clinical illness in the course of infection while others exposed to the same microbe remain unharmed. The laboratory revealed that single-gene inborn errors of immunity in children may confer severe and selective vulnerability to certain infectious illnesses, whereas corresponding infections in adults result more from complex inheritance. This work not only blurs the distinction between patient-based Mendelian genetics and population-based complex genetics but also provides experimental support for a unified genetic theory of human infectious diseases.

Membership Type

International Member

Election Year


Primary Section

Section 43: Immunology and Inflammation

Secondary Section

Section 41: Medical Genetics, Hematology, and Oncology