Shokrollah Elahi joined the School in 2014. He obtained several degrees from the Tehran University of Medical Sciences, Iran, and his PhD in Immunology from the Newcastle University in Australia. Elahi moved to Canada and did his first post-doctoral fellowship at Vaccine and Infectious Disease Organization (VIDO) followed by second post-doctoral fellowship at the Center for Infectious Diseases Research affiliated with the University of Washington (Seattle). Later on as a staff scientist, he continued his research in HIV/AIDS pathogenesis. Finally, he moved to Cincinnati Children's Hospital Medical Centre where he investigated the mechanism underlying the susceptibility of neonates to infectious disease.
Elahi’s laboratory has a diverse research program:
- HIV-pathogenesis with particular interest in understanding the mechanisms that enable some HIV-infected individuals to control the viral replication. These individuals are defined as long-term non-progressors (LTNPs) or elite controllers. Unveiling host factors and immune responses for such phenomenon will likely provide insight for the development of novel therapeutic interventions and more rational design for therapeutic vaccine components and functional cures.
- Understanding the immune pathogenesis of neonatal infection. The team’s recent finding fundamentally changed how we look at neonatal susceptibility to infection by suggesting it is caused by active immune suppression during this developmental period, as opposed to the immaturity of immune cells. This discovery highlights the critical role of temporal immune suppression to quench the excessive inflammation induced by abrupt colonization with commensal microorganisms after parturition.
- The other avenue of research in Elahi’s laboratory is to map the mechanism(s) and pathways of cytotoxic T lymphocytes (CTLs) exhaustion in chronic conditions such as viral infections and cancer. In particular my laboratory focuses on the role of immune checkpoints in chronic conditions. In cancer and in chronic viral infections, CTLs receive persistent molecular signals from antigens or inflammation. This is often associated with deteriorating CTL function and exhaustion. Exhausted CTLs express multiple inhibitory receptors (immune checkpoints) that render patients unable to mount an effective CTL response against tumours and chronic viral infections. We aim to better understand CTL exhaustion in order to develop novel immunotherapies against chronic infections and cancer.