Djamel Nehar-Belaid

Background

I am an immunologist with ~13 years of experience in cellular immunology, computational biology, and transcriptomic data analysis. Utilizing my hybrid research profile with both bench (wet lab) and bioinformatics (dry lab) expertise, I have focused my efforts towards understanding immune system dynamics in different contexts including cancer, pregnancy, aging, and autoimmune diseases. Currently, I am a Research Scientist at The Jackon laboratory for Genomic Medicine (Ucar lab).

Postdoctoral work: Banchereau lab - JAX-GM (Farmington, CT, USA)

Within the Banchereau lab (2016-2021), I have been developing computational pipelines to analyze human blood cell transcriptomic data at the single cell resolution in different contexts, including autoimmunity (e.g. systemic lupus erythematosus; SLE) and aging. My initial work sought to resolve the transcriptional signatures described decades ago in SLE using cutting-edge single cell RNA-seq approaches. This analysis allowed a more accurate classification of lupus patients based on specific cell types. This first direct comparison of childhood and adult SLE confirmed the presence of similar transcriptional patterns across age groups and enabled patient classification according to disease activity. Also, in collaboration with the Akbar lab (at UCL, London, England) we could demonstrate that senescent CD8+ T cells can develop NK cell-like features over time, a process that was regulated by the stress-sensing proteins called sestrins.

Ph.D. work - Early research: Klatzmann lab (Paris, France)

During my predoctoral training (Klatzmann lab; University Pierre & Marie Curie, Paris, France; 2010-2016), I focused on understanding why embryos and tumors expressing foreign antigens were not rejected by the immune system. Using murine models (pregnant mice and mice injected with different tumor models), I demonstrated that a specific CD4+ T cell population, the regulatory T cells (Tregs), orchestrates similar immune evasion mechanisms in both fetuses and tumors. Using both transcriptomic profiling and flow cytometry analysis of the tumor microenvironment, we demonstrated that co-silencing of TGF-β and VEGF led to a substantial spontaneous tumor eradication rate and the combination of their respective inhibitory drugs was synergistic. A collaboration with the Aryee lab (Massachusetts General Hospital & Harvard Medical School) allowed us to confirm our findings on the similarities between tumor and fetal development in humans.