Gil Katz

Gil Katz PhD in immunology and tumor immunology from the Hebrew university in Jerusalem focusing on activating and inhibitory receptors expressed on Natural Killer (NK) cells that are involved in tumor cell recognition.

Visiting fellow position at National Institutes of Health (NIH) studying T cell development and the interplay between T cell receptor (TCR) signaling and cytokine signaling.

Research fellow position at Uniformed Services University of the Health Sciences (USUHS) investigating the mechanisms of apoptosis induction in restimulated T cells and pathologies related to defects in T cell apoptosis. At USUHS also served as basic science instructor in immunology in research training programs.

Worked as senior scientist and project leader in biotech companies developing cancer immunotherapies, including NK-CAR (Cimeric Antigen Receptor), immune checkpoint inhibitors, and T cell engagers.

Scientific activities in 2024

At IMBM working as Biomedical Project Manager responsible for creating and expanding scientific collaborations, and as key knowledge person in immunology and cell biology.

Publications

    1. Katz G, Voss K, Yan TF, Kim YC, Kortum RB, Scott DW, Snow AL. 2018. FOXP3 renders activated human regulatory T cells resistant to restimulation-induced cell death by suppressing SAP expression. Cell Immunol. 327:54-61.
    2. Katz G, Pobezinsky LA, Jeurling S, Shinzawa M, Van Laethem F, Singer A. 2014. T cell receptor stimulation impairs IL-7 receptor signaling by inducing expression of the microRNA miR-17 to target Janus kinase 1. Sci Signal. 7:ra83.
    3. Katz G, Krummey SM, Larsen SE, Stinson JR, Snow AL. 2014. SAP facilitates recruitment and activation of LCK at NTB-A receptors during restimulation-induced cell death. J Immunol. 192:4202-9.
    4. Xuguang T, Erman B, Alag A, Mu J, Kimura M, Katz G, Guinter T, McCaughtry T, Etzensperger R, Feigenbaum L, Singer DS, Singer A. 2013. Foxp3 transcription factor is proapoptotic and lethal to developing regulatory T cells unless counterbalanced by cytokine survival signals. Immunity. 38:1116-28.