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Figure 1 Single cell sequencing of B cells from NMDA receptor antibody encephalitis

Single cell RNA and B cell receptor (BCR) sequencing data showed intratumoral autoimmunization: cell type-specific clusters (top left), BCR constant regions (top right) and variable region mutation rates (bottom). Modified from doi: 10.1093/brain/awac088

Adam Handel

Honorary Clinical Lecturer in Neurology

  • Post-doctoral Bioinformatician

Current Research

My current research aims to understand clinical features and the molecular immunopathogenesis of neuroinflammatory conditions, with a particular focus on autoimmune encephalitis. I have identified clinical features characterizing several types of neurological conditions mediated by autoantibodies. I have generated high-throughput single-cell sequencing libraries from multiple tissues, including peripheral blood and cerebrospinal fluid, in patients with autoantibody-mediated CNS diseases (Fig. 1).

My research also explores different aspects of thymic biology in both normal development and with genetic disruption of thymic epithelial cell function (Fig. 2). I used functional genomics methods to investigate the mechanisms underlying thymic function and other aspects of adaptive immunity. Through a combination of single cell sequencing and multiplexed spatial proteomics, I aim to understand how T cells with autoreactive against CNS antigens can escape thymic negative selection.

Previous Research

I used induced pluripotent stem cell models to assess the cellular phenotype of cortical neurons in the context of normal development and neurodegenerative disease. As part of these projects, I applied single cell PCR and sequencing methodologies to in vitro models of corticogenesis. I also analyzed chromatin accessibility data to investigate the genetic mechanisms underlying susceptibility to neurological disease. I collaborated on genomic method development to apply capture sequencing to ultra-low and single cell libraries.

My pre-doctoral research focused on the interactions between genetic and environmental factors in determining susceptibility to multiple sclerosis. I applied a variety of statistical models to epidemiological datasets to dissect out the contribution of latitude, month-of-birth, infectious mononucleosis, vitamin D and smoking to multiple sclerosis prevalence and incidence. I used functional genomics methods, including transcriptomics and ChIP-seq to implicate several molecular mechanisms likely to underlie the effect of vitamin D on the immune system.

Key publications

Recent publications

More publications

Figure 2 Single cell ATAC-RNA-seq multiomics in human thymus

A link plot showing key enhancer and promoter loops regulating SOX10 expression in human thymic mesenchymal cell populations. Modified from doi: 10.1126/sciadv.abm9844