The Harder lab has a long-standing interest in understanding the developmental programs guiding monocyte, macrophage, neutrophil and dendritic cell production from hematopoietic stem and progenitor cells. We are particularly interested in delineating the key phagocyte subsets, genes, and signalling pathways associated with chronic inflammatory diseases such as cancer, inflammatory bowel disease, heart disease, obesity, aging, and neurodegeneration, as recent studies by us and others have shown that phagocytes play key roles in each of these diseases.

Our studies have revealed the widespread impact that chronic inflammatory diseases have on these lineages of immune cells and our recent work has focused on understanding how key cytokines and signalling pathways control phagocyte fate and function. We contend that new treatments for these diseases will require a better understanding of phagocyte biology associated with disease, and will entail new strategies to target phagocytes with drugs, biologics, genetic modification strategies, or adoptive cell therapy approaches.

We employ a variety of cutting-edge techniques in our studies including systems biology single cell proteomic and transcriptomic technologies (CyTOF, scRNA-seq, CITE-seq) that rely on computational machine learning platforms to allow high dimensional, deep phenotyping of tens of thousands of individual cells in health and disease, simultaneously. Other technologies used in the lab include: genetically engineered mouse models, tissue culture/cellular immunology assays, flow cytometry, immunohistochemistry, molecular biology, CRISPR/Cas9 mutagenesis, siRNA technology, RNA-seq, new adoptive cell therapy approaches, and most recently lipid nanoparticle (LNP) mediated mRNA delivery in vivo.