Amir Horowitz

Amir Horowitz

Company: Icahn School of Medicine at Mount Sinai

Job title: Professor

Bio:

Amir Horowitz, PhD is an Assistant Professor of Oncological Sciences and a member of the Precision Immunology Institute and the Tisch Cancer Institute at the Icahn School of Medicine at Mount Sinai.

Central to his studies is how immunogenetic variation of HLA, KIR and CD94:NKG2A genes governs the education of human NK cells and regulates their ability to function within dynamic environments. A central goal of his lab’s research is to investigate the effects of genetic variation on the effector and immunoregulatory roles of NK cells in patients with cancer receiving immunotherapies. Throughout my training, he has developed expertise in immunology of infectious diseases and cancer, evolutionary and population immunogenetics, structural biology, and epidemiology. He has cultivated long-standing collaborations with leading scientists in the field of NK cell immunology and HLA genetics and currently have studies focused across settings of hematologic and solid tumor malignancies. His work has contributed to developing an understanding of adaptive NK cells and their roles in microbial infections and following vaccination and hematopoietic cell transplantation (HCT). He was the first person to demonstrate adaptive roles for human NK cells in vaccine settings as a strategy to potentiate T cell memory. He also pioneered the first studies of human NK cells by mass cytometry (CyTOF) and demonstrated an enormous breadth of phenotypic diversity and functions associated with specific HLA class I and KIR backgrounds. This research has led to the identification and characterization of numerous NK cell subset populations with unique activity and antiviral (and anti-tumor) potential. His laboratory uses tools such as CyTOF, tissue imaging mass cytometry, single-cell RNA sequencing, Olink proteomics, next generation sequencing and computational analytics. They study how HLA class I mediated education and inhibition of NK cells and tumor-derived mutations affecting HLA class I expression and antigen presentation determines sensitivity of NK cells and CD8 T cells to tumor cells, immunosuppressive elements produced within the tumor microenvironment and the capacity to potentiate anti-tumor CD8 T cell activity in response to immune checkpoint blockade therapy. 

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