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A headshot photo of Edwin Wan.

Edwin Wan

Assistant Professor

Contact Information

Phone
304-293-6293
Address
PO Box 9177
64 Medical Center Drive
Morgantown, WV 26506

Affiliations

  • Department of Microbiology, Immunology, & Cell Biology
  • Department of Neuroscience
  • Rockefeller Neuroscience Institute

Graduate Training

  • Cancer Immunology & Pharmacology, City University of Hong Kong

Fellowships

  • Immunology, National Institutes of Health
  • Immunology, Duke University Medical Center

Research Interests

My laboratory is interested in two areas of research:

Elucidating the role of cytokine signaling in the pathogenesis of multiple sclerosis

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. An active, responsive immune system is certainly important as patients with immunodeficiency often develop cancers, and are frequently subjected to infections. 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.

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.

Mechanistic study of stroke-induced immune suppression and identification of immune modulatory targets for post-stroke pneumonia

Approximately 30% of stroke patients suffer from post-stroke pneumonia, which is the major cause of mortality from this disease. Recent multi-center clinical studies suggested that prophylactic antibiotic treatments do not reduce the incidence of post-stroke pneumonia nor mortality. Moreover, the emergence of antibiotic resistant bacteria renders the “gold standard” antibiotic treatments ineffective. Therefore, novel therapeutic strategies are needed to improve clinical outcomes.

Using mouse models of focal brain ischemia coupled with Pseudomonas aeruginosa infection, the overall goal of my research is to 1) determine the cellular and molecular profiles of immune cell niches in the lungs after focal brain ischemia induction; 2) elucidate the immune suppressive mechanisms following ischemic stroke event; and 3) identify key cytokines and chemokines that contribute to post-stroke pneumonia.

Overall, this study will elucidate the immune cell types involved and the underlying mechanisms that govern post-stroke pneumonia, with the goal of identifying novel therapeutic targets and improving clinical outcomes.

Recent Publications

Representative Publications

 
1. Monaghan KL*, Farris BY*, Zheng W, Wan ECK# (2020). Characterization of immune cells and proinflammatory mediators in the pulmonary environment. Journal of Visualized Experiments 160, e61359 doi:10.3791/61359. (*Co-first authorship; #Corresponding author)
 
2. Monaghan KL, Wan ECK# (2020). The role of granulocyte-macrophage colony-stimulating factor in murine models of multiple sclerosis. Cells 9:611 doi:10.3390/cells9030611. (#Corresponding author)
 
3. Monaghan KL, Zheng W, Hu G#, Wan ECK# (2019). Monocytes and monocyte-derived antigen-presenting cells have distinct gene signatures in experimental model of multiple sclerosis. Frontiers in Immunology 10:2779 doi:10.3389/fimmu.2019.02779. (#Corresponding author)
 
4. Farris BY, Monaghan KL, Zheng W, Amend CD, Hu H, Ammer AG, Coad JE, Ren X, Wan ECK# (2019). Ischemic stroke alters immune cell niche and chemokine profile in mice independent of spontaneous bacterial infection. Immunity, Inflammation and Disease 7:326-341 doi:10.1002/iid3.277. (#Corresponding author)
 
5. Palle P*, Monaghan KL*, Milne SM, Wan ECK# (2017). Cytokine signaling in multiple sclerosis and its therapeutic applications. Medical Sciences 5:23 doi:10.3390/medsci5040023. (*Co-first authorship; #Corresponding author)
 
6. Wan ECK*, 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)
 
7. Wan ECK, 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-1 production in conventional dendritic cells. Nature Communications 6:7988 doi: 10.1038/ncomms8988.
 
8. Wan ECK*, 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)
 
9. Wan ECK, Oh J, Li P, 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.