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.
- Understanding the mechanism(s) and pathways associated with CTL exhaustion in chronic conditions.
- Defining cellular and molecular changes after immune checkpoint blockade in melanoma patients.
- Determining the role of CD71+ erythroid cells in immune regulation.
- Identifying and testing novel immune checkpoint blockers for efficacy and safety in cancer patients.
- Delineating early immunological events at the mucosal sites such as oral cavity and gastrointestinal tract that modulate HIV susceptibility (eg. mucosal inflammation, microbial flora).
- Investigating the mechanism associated with accelerated aging in HIV infected individuals and how to prevent it.
HIV pathogenesis, Cancer Immunotherapy, Immunoregulation, Immune checkpoints, Neonatal immunology, Microbiome, Cancer
Isobel Okoye Ph.D., Research Associate
Lai Xu M.Sc, Research Assistant and The Laboratory Manager
Olaide Oyegbami Ph.D., Research Assistant
Garett Dunsmore, Graduate student
Najmeh Bozorgmehr, Graduate student
Shima Shahbaz, Graduate student
Siavash Mashhouri, Graduate student
Elianna Perez Rosero, Gradate student
Mai Huynh, Undergraduate student
Abdul Jamro, Undergraduate student
Crystal Du, Undergraduate student
- Elahi S., Ertelt M. J., Kinder J., Jiang T. T., Zhang X., Xin L., Chaturvedi V., Strong S. B., Qualls J., Kalfa A. T., Shaaban A., and Way SS. Immunosuppressive CD71+erythroid cells compromise neonatal host defense against infection. Nature, 2013 Dec 5;504(7478):158-62.
- Elahi S., L. Dinges. W., Lejarcegui N., Laing J. K., Collier C. A., Koelle D., M. McElrath M. J., and Horton H. Protective HIV-specific CD8+ T cells evade regulatory T cells suppression. Nature Medicine 2011 Jul 17;17(8):989-95. “Selected by Faculty 1000 as a must read article"
- Elahi S., Toshiro N., Hirashima M., and Horton H. Galectin-9 binding to Tim-3 renders human activated CD4+ T cells less susceptible to HIV-1 infection. Blood 2012 May 3;119(18):4192-204.
- Shahbaz S., Bozorgmehr N., Petya Koleva P., Namdar A., Jovel J. and Elahi S.* CD71+VISTA+ erythroid cells promote the development and function of regulatory T cells through TGF-b. Journal of PLOS Biology 2018 Dec 14;16(12):e2006649. doi: 10.1371/journal.pbio.2006649.
- Elahi S.* Neglected Cells: Immunomodulatory role of CD71+ Erythroid Cells. Trends in Immunology, 40-30 (2019) p2.
- Namdar A., Dunsmore G., Shahbaz S., Koleva P., Xu L., Jovel J., Houston S. and Elahi S*. CD71+ erythroid cells exacerbate HIV-1 susceptibility, mediate trans-infection and harbour infective viral particles. mBio. 2019 Nov 26;10(6).
- Dunsmore G., Koleva P., Ghobakhloo N., Sutton R. T., Ambrosio L., Meng X., Hotte N., Nguyen V., Madeson L. K., Dieleman L., Huang V. and Elahi S.* Lower Abundance and Impaired Function of CD71+ Erythroid Cells in Inflammatory Bowel Disease Patients During Pregnancy. Journal of Chron’s and Colitis 2018 Oct 1.doi:10.1093/ecco-jcc/jjy147.
- Meng X., Dunsmore G., Koleva P., Elloumi Y., Wu R Y., Sutton T R., Ambrosio L., Hotte N, Nguyen V., Madsen L K., Dieleman A L., Chen H., Huang V., and Elahi S.* The profile of human milk metabolome, cytokines and antibodies in inflammatory bowel diseases versus healthy mothers and potential impact on the newborn. Journal of Chron’s and Colitis 2018 Nov 12. Doi:10.1093/ecco-jcc/jjy186.
WCHRI Innovation Grant, Principal Investigator, $50,000 (2018-2020)
CIHR, Foundation Scheme, Principal investigator, $1,100,000 (2016-2021)
WCHRI Innovation Grant, Principal Investigator, $50,000 (2016-2018)
Alberta Cancer Foundation, Co-investigator, $200,000 (2018-2020)
Li Ka Shing Institute of Virology, Principal Investigator, $40,000 (2019-2020)
CIHR Salary award, Principal Investigator $300,000 (2016-2021)
CIHR New Investigator Award in Maternal, Reproductive, Child and Youth Health $225,000 (2017-2020)
CIHR, defining molecular mechanisms allowing polyfunctionality and regulatory T cells evasion during chronic HIV-1, Principal investigator (100%) $450,000 (2014-2017)
Alberta Cancer Foundation/Alberta Virology Institute, Developing novel cancer immunotherapy drugs: a multidisciplinary team. Co-leader $5,400,000 (2015-2020)
WCHRI Innovation Grant, Principal investigator (100%) $50,000 (2014-2016)