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Xiao-Qing Wei

Dr Xiao-Qing Wei

Senior Lecturer in Immunology, School of Dentistry

School of Dentistry

Available for postgraduate supervision


Dr. Xiao-Qing Wei is a Senior Lecturer in Immunology. His research focuses on the study of cytokine function in infection and immunity. He is one of the pioneer researchers in the identification of IL-35 and its application as an immune suppressing molecule in rheumatoid arthritis. His work has significantly contributed to the understanding of the mechanism of autoimmune and inflammatory diseases.

































Research interests

Cytokines play a pivotal role in controlling the outcome of infectious and inflammatory diseases by regulation of host innate and adaptive immunity. My research has focused on the understanding of the role of some important pro-inflammatory cytokines, such as IL-15, IL-18, IL-12, IL-23, IL-27 and the novel anti-inflammatory cytokines, IL-34 and IL-35, in disease processes in order to find practical ways to regulate host immune responses for treatment. Inflammatory cytokines promote host immunity against pathogen invasion and tumour formation. However, over reaction also results in autoimmune and inflammatory diseases, such as rheumatoid arthritis and periodontal diseases. Host cells produce anti-inflammatory cytokines to avoid this over-reaction. One of these important anti-inflammatory cytokines is IL-35. I am one of the pioneer researchers who discovered IL-35 and identified its anti-inflammatory role using a mouse rheumatoid arthritis model. My research is continuing to understand the role of IL-35 in other human diseases such as candidosis, tumour development and neuronal degeneration. Through understanding the biological mechanisms of IL-35 in human diseases, development of therapies to treat those human diseases may be achieved.

Tissue resident macrophages occupy 5-10% of the cell component of tissues and play important roles in the removal of dead cells and cytokine production during disease processes. Tissue macrophages are highly heterogeneous and exhibit plasticity. Inflammatory tissues with higher pro-inflammatory cytokines will induce macrophages to their M1 phenotype, while in an anti-inflammatory environment with higher levels of growth factors and anti-inflammatory cytokines, conversion to the M2 phenotype is favoured. My research aims to determine how the tissue environment modulates this macrophage phenotype transition and how these macrophages contribute to the outcome of human diseases, including candidosis, tumour development, neuron degeneration and tissue repair.Vaccines are effective tools in preparing the host immune system for protection against pathogen invasion. Cytokines also play a key role during vaccination. T cell development in a certain cytokine environment determines the types of immunity,i.e.cellular or humoral immunity. Many failures of vaccination result from the stimulation of the wrong type immune responses. Cell mediated immunity is absolutely critical for the success of some vaccination. Currently I am working on developing a vaccination process that combines cytokines with physical stimulation, nanoparticle and microneedle delivery system. The novel protocol and device for vaccination should be highly benefitial in promoting human health.

Current Projects

Studying the role of novel cytokines, IL-35, in the regulation of host immune response against tumour and yeast infection.

Studying the role of novel cytokine IL-35 in atheroscerosis. 

Studying the influential role of cytokine IL-35 in pneumonia and covid-19 infection. 


Apart from research undertaken at the School of Dentistry, Cardiff University, Dr. Wei also has responsibility for teaching on the oral ecosystem course for year 2 BDS students. He is involved in the examination and assessment of this course. Dr Wei also has an assessment role in Team Based Learning (TBL). Recently, he has took a model lead role in the mentorship of year 2 students post presentation and assessment. Dr Wei also supervises projects of final year BDS students. He is also helping in coordination of final year research project in dental school. 


Dr. Xiao-Qing Wei graduated in medicine from the Medical School of Peking University (Beijing Medical University) in Beijing, China, and worked in the Beijing Hepatitis Research Institute of Youan Hospital, where he carried out research on infectious diseases, particularly hepatitis. He joined an immunology group at the University of Glasgow to investigate the role of inducible nitric oxide (iNOS) in infection and immunity and gained a PhD at the University of Glasgow. His post-doctoral research has concentrated on investigating the role of some important cytokines such as IL-15, IL-18, IL-23 and IL-27 in T cell development. The primary aim of his research in infectious and autoimmune diseases is to develop a practical anti-cytokine therapy to treat the inflammatory disorder, such as rheumatoid arthritis (RA). As a Senior Research Fellow, his research was supported by Arthritis Research UK to study the function of IL-18 and its receptors in RA. During that time, Dr Wei applied his research to studying the mechanism of anti-inflammation. Dr Wei is a pioneer researcher in the discovery of IL-35 and demonstrated its immune suppressing role in the treatment of the joint inflammation in mouse collagen induced arthritis model, which closely mimics rheumatoid arthritis in humans. His IL-35 study contributed significantly to the understanding of inflammatory disease mechanisms and may also benefit in future therapies of human autoimmune and inflammatory disorders. He was first appointed as a Lecturer in School of Dentistry, Cardiff University and was recently promoted to Senior Lecturer. Dr Wei's current research now focuses on the study of the role of novel IL-34 and IL-35 cytokines in the regulation of host immunity, particular concerning tissue macrophages andCandida infection, tumour survival, skin vaccine and skin/spinal wound healing. He is also interested in studying the functions of cytokine associations with mineralised tissue destruction related to RA, osteoarthritis and periodontal diseases.

Honours and awards

MB BCh, Medical School of Peking University (Beijing Medical University)PhD, University of Glasgow


Title: Molecular Biology and Protein Science: Characterisation of IL-35 receptors for cytokine binding to create decoy soluble receptor for tumour therapy

Interleukin-35 (IL-35) is a new cytokine member of IL-12 family and has an immune suppressive role in inflammatory disorders, including wound healing and tumour development. Macrophages exhibit plasticity for changing their phenotypes to their tissue environments. For example, M1 inflammatory macrophages arise in inflammation for tumoricidal effects or M2 anti-inflammatory macrophages occur in resolving inflammation during tumour growth and metastasis. We have recently demonstrated that IL-35 can convert M1 into M2 macrophages to promote tumour development. Both tumour and infiltrated regulator T cell (Treg) produce IL-35. Higher IL-35 expression in tumours result in tumour growth and metastasis, which is associated M2 macrophage expansion in tumours. IL-35 binds to gp130 and IL-12Rb2 for its biological activity. IL-35 can use gp130 homodimer, IL-12Rb2 homodimer and gp130/IL-12Rb2 heterodimer to induce its biological activity by phosphorylation of STAT1, 3, and 5 gene transcription factors respectively. The detail mechanism(s) of how IL-35 suppresses immune responses in inflammation remain unknown. Combination of the receptors usage for a higher affinitive and specific IL-35 binding was also not studied. The hypothesis of this proposed project is that heterodimer of gp130 and IL-12Rβ2 provides a highest affinity binding to IL-35. Decoy soluble gp130/IL-12Rβ2 will block IL-35 specifically which can be used in tumour therapy. This project will characterise the IL-35 receptor for its ligand binding followed by constructing a soluble decoy IL-35 receptor to block IL-35 biological activity. This specific IL-35 blocker may be also used in study the IL-35 in other diseases, such as atherosclerosis and autoimmune disorders.