Research groups
Ping Zhang
Senior Biostatistical Researcher
Genetics and Functional Genomics
Human genetic variation underlying disease susceptibility is an important determinant of inter-individual variability in disease severity and drug response through regulatory effects on gene expression and functional activity. However, translating disease-associated loci into actionable therapeutic targets remains challenging due to difficulties in (i) identifying causal variants, (ii) defining context-specific effects and (iii) establishing mechanistic links to cellular phenotypes and clinical outcomes.
My research dissects how genetic and epigenetic variation regulates human immune responses, with a focus on sepsis-associated inflammation, immune tolerance and the crosstalk between innate and adaptive immunity. I integrate multi-omics profiling, eQTL mapping, CRISPR-based perturbation and advanced computational analyses to identify causal genetic mechanisms underlying disease-relevant immune phenotypes.
I hope to build on the work to translate genetic and epigenetic insights into new biomarkers and therapeutic strategies to improve patient stratification and treatment response.
Background
I earned my PhD in Cancer Biology at Heidelberg University, where I studied the genetic and molecular mechanisms regulating the tumour suppressor p53.
Recent publications
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Context-specific regulatory genetic variation in MTOR dampens neutrophil-T cell crosstalk in sepsis, modulating disease
Preprint
Zhang P. et al, (2025)
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Evolution of T cell responses in the tuberculin skin test reveals generalisable Mtb-reactive T cell metaclones
Preprint
Turner C. et al, (2025)
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eQTLs identify regulatory networks and drivers of variation in the individual response to sepsis.
Journal article
Burnham KL. et al, (2024), Cell genomics
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New role of fat-free mass in cancer risk linked with genetic predisposition.
Journal article
Harris BHL. et al, (2024), Scientific reports, 14
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Mapping the epigenomic landscape of human monocytes following innate immune activation reveals context-specific mechanisms driving endotoxin tolerance.
Journal article
Amarasinghe HE. et al, (2023), BMC genomics, 24