Microbiology, Immunology, & Cell Biology; Center for Basic & Translational Stroke Research
Cancer Immunology & Pharmacology, City University of Hong Kong
Immunology, National Institutes of Health
Immunology, Duke University Medical Center
Research profile: https://www.researchgate.net/profile/Edwin_Ck_Wan
Our immune system needs to be in a perfect balance for keeping us healthy, and this balance is maintained by a group of proteins named “cytokines”. Cytokines are signaling molecules used to communicate between various immune cell types, which are critical not only for their development, but also for ensuring proper immune responses are triggered when required (see Wan and Leonard, Encyclopedia of Immunobiology 2016). An active, responsive immune system is certainly important as patients with immunodeficiency often develop cancers, and are frequently subjected to infections (see Wan et al., PNAS 2015). However, excessive immune responses are also not desirable, as they would lead to immunopathology. Examples are autoimmune diseases caused by over-reactive immune cells that recognize and attack our own body (see Wan et al., Immunity 2013; Wan et al., J Immunol 2016).
Multiple sclerosis (MS) is an autoimmune disease that the over-reactive immune cells attack the central nervous system (CNS). This attack causes severe inflammation, leading to irreversible damages of the CNS. Current therapeutic strategies aimed to reduce the frequency of relapses (attacks) but are unable to cure the disease. Improper production of certain cytokines, such as GM-CSF, IL-17 and IL-23 significantly correlates with the pathogenesis of MS but exactly how they do it, particularly what immune cell types and signaling pathways involved are not well defined. The overall goal of my research is to 1) identify cytokines and underlying mechanisms that govern the pathogenesis of multiple sclerosis, and neuroinflammation in general, using pre-clinical animal models; 2) explore novel inhibitors that target signaling molecules responsible for triggering neuroinflammation by high throughput screening; and 3) decipher gene expression profiles and functional abnormality of immune cells isolated from MS patients.
These studies will not only improve our understanding on how improper control of immune cell activation leads to neuroinflammation, but also have potential clinical impacts on MS treatments.
Dr. Wan's research group is currently recruiting motivated Postdoctoral Fellows, Research Assistants, and Graduate Students who have broad interest in studying signaling pathways underlying the pathogenesis of autoimmune and infectious diseases. Please email a cover letter explaining research background and interest, and a CV to firstname.lastname@example.org
- Wan CK*, He C*, Sun L, Egwuagu CE, Leonard WJ (2016). Cutting Edge: IL-1 receptor signaling is critical for the development of autoimmune uveitis . Journal of Immunology 196:543-546. (*Co-first authorship)
- Wan CK, Li P, Spolski R, Oh J, Andraski AB, Du N, Yu Z, Dillon CP, Green DR, Leonard WJ (2015). IL-21-mediated non-canonical pathway for IL-1β production in conventional dendritic cells . Nature Communications 6:7988 doi: 10.1038/ncomms8988.
- Wan CK*, Andraski AB*, Spolski R, Li P, Kazemian M, Oh J, Samsel L, Swanson PA II, McGavern DB, Sampaio EP, Freeman AF, Milner JD, Holland SM, Leonard WJ (2015). Opposing roles of STAT1 and STAT3 in IL-21 function in CD4+T cells. PNAS 112: 9394-9399.(*Co-first authorship)
- Wan CK, Oh J, Peng L, West EE, Wong EA, Andraski AB, Spolski R, Leonard WJ (2013). The cytokines IL-21 and GM-CSF have opposing regulatory roles in the apoptosis of conventional dendritic cells. Immunity 38:514-527.
- Wan CK and Leonard WJ (2016). γc family cytokines: role in immune cell development and function. In Michael JH Ratcliffe, Encyclopedia of Immunobiology, Volume 2, pp. 509-518. Cambridge, MA: Academic Press.