Liye Chen

Dr Liye Chen originally trained in Medicine at HuaZhong University of Science and Technology. He subsequently developed his interest in rheumatology research during his Arthritis UK-funded PhD (2009-2013, Paul Bowness Group, University of Oxford), during which he described functional explanations for the genetic association of ERAP1 with HLA-B27⁺ spondyloarthritis (SpA). He then worked as a postdoctoral researcher (2014–2019, University of Oxford), and extended this line of work to show how ERAP1 regulates the HLA-B51 immunopeptidome and demonstrated that variation at amino acid position 97 confers SpA risk by enhancing cell-surface expression of aberrant β2m-free HLA-B heavy chains. In parallel, he investigated T-cell biology in SpA, contributing to reports showing regulation of Th17 responses by miR-10b-5p and JAK kinases, while also contributing to discoveries on GPR65 regulation of GM-CSF⁺ CD4⁺ T cells and IRF5 regulation of CD8⁺ IFNγ production. 

Supported by an Arthritis UK Fellowship, he established his laboratory in 2019 in NDORMS, University of Oxford. His lab's focus has been on the immune mechanisms within inflamed synovial tissue, an underexplored compartment in spondyloarthritis (SpA). He utilised a three-step research strategy: (1) discovery of novel biology directly in synovial tissue, (2) in vitro modeling using primary human cells, and (3) application of CRISPR-based screening platforms to identify key regulators and therapeutic targets. A key outcome of this approach was our recent discovery that CD4⁺ tissue-resident memory Th17 (TRM17) cells are the major source of IL-17A in SpA synovium, regulated by the epigenetic factor BRD1. This represents a paradigm shift - moving the field’s focus from circulating immune cells to tissue-resident “factories” of inflammation. 

Current core research themes in his lab include:

• Tissue-resident memory T Cells in health and disease

• Role of myeloid cells in inflammation and resolution

• Developing high-throughput CRISPR screens for primary immune cells