Jerry (Chenglong) Wang

    Find Jerry (Chenglong) Wang on

    PhD Student

    Chenglong (Jerry) Wang is an immunology PhD candidate in the Centre for Immunology and Infection Control at QUT. He received a bachelor’s degree in pharmaceutical science in China. He went to Australia for master’s degree of molecular biology at University of Queensland in 2018. He found a great interest in immunology during the study in molecular biology, so at the November in 2020 he started a PhD journey at QUT with Dr. Stephen Daley. His research topic is self-peptide antigenicity in T-regulatory cell development and autoimmunity.

    Self-peptide antigenicity in T-regulatory cell development and autoimmunity

    The risk of many organ-specific autoimmune diseases is influenced by alleles in the major histocompatibility complex (MHC). MHC proteins present peptide antigens to T cells. Risk-associated MHC alleles are thought to increase the probability of self-peptide presentation to pro-inflammatory T cells, but an alternative possibility is that they fail to present a self-peptide to regulatory T cells (T-regs). This study will test whether the antigenicity of a self-peptide presented by a risk-associated MHC allele affects T-regs development and susceptibility to autoimmune disease. A humanised mouse model of renal autoimmune disease is used, where the key peptide/MHC self-antigen has been defined and structurally characterised. To assess peptide antigenicity, splenocytes from naïve or peptide-primed mice were labelled with proliferation dye and cultured with the wild-type peptide or variant peptides in which the exposed position 5 (P5) residue was substituted to other 19 amino acids. The wild-type peptide induced a relatively low amount of pro-inflammatory cytokine synthesis and CD4+ T-cell proliferation compared to some variant peptides, with the highest T-cell activation induced by a variant peptide with tryptophan at P5. The amino acid at P5 has a marked effect on the antigenicity of a self-peptide targeted by T cells in renal autoimmune disease. Introducing a tryptophan at P5 produces a more antigenic complex which, if expressed as a self-antigen, may alter antigen-specific regulatory T cell development in the thymus and susceptibility to renal autoimmune disease. From this project we expect new insights into the immunogenetic basis of autoimmune disease.