UCR

Institute for Integrative Genome Biology



Members


Emma WilsonEmma H. Wilson

Assistant Professor

Mailing Address:

Biomedical Sciences
Webber Hall /1237
University of California
Riverside, CA 92521

Phone: (951) 827-4328
Fax: (951) 827-4437
Email: emmaw@ucr.edu

Website

Degree(s):

PhD Immunology 2002 University of Strathclyde, Glasgow, Scotland, UK
BSc Ecology 1997 University of Dundee

College/Division Affiliation:

Division of Biomedical Sciences

Center/Inst Affiliation(s):

Center for Glial Neuronal Interactions
Center for Disease Vector Research

Areas Of Expertise:

Immune Response to Toxoplasma gondii; Cell Migration in the Brain

Research Summary:

Studying Infection Induced Inflammation in the CNS
Toxoplasma cyst

Electron micrograph of a toxoplasma cust containing individual slow replicating badyoites (image courtesy of David Ferguson, Oxford)

The primary focus of the lab is the immune response in the brain following Toxoplasma gondii infection. This is a common parasitic infection of many mammals including humans where prevalence is 10-30% in the USA and up to 80% in parts of Europe and South America. Infection with this parasite leads to an acute systemic inflammatory response that is controlled resulting in a chronic phase of infection where the parasite is maintained predominantly as a slow replicating form in the CNS. In most cases this results in no overt pathology however in the absence of an appropriate immune response, the parasite will reactivate leading to Toxoplasmic encephalitis (TE) a disease that is often fatal if left untreated.

Thus, T. gondii infection is a rare example of a finely tuned immune response in the brain where there is a balance between control of the parasite and immunopathology. Understanding the mechanisms that control this balance may improve our ability to control an inappropriate immune response in the CNS.

 

The importance of CNS resident cells during T. gondii infection
Brain section with T. gondii infection

Brain section illustrating pathology induced by infiltrating leukocytes during T. gondii infection

Although the susceptibility of patients with acquired immunodeficiencies illustrates the importance of an adaptive T cell response in controlling T. gondii, previous studies have suggested that the immune response to Toxoplasma at the chronic stage of infection is localized to the brain implying CNS intrinsic mechanisms of control.

The activation of astrocytes is the first sign of infection in the brain. These cells play an important structural role and maintain the health of neurons however they also have the capacity to act immunologically including an ability to produce chemokines, cytokines and to present antigen. By targeting specific immune functions of astrocytes, their role during T. gondii infection can be studied in vitro and in vivo using a large array of immunological techniques including live imaging of cells. In addition, collaborations with Dr. Monica Carson at UCR focus on the role of microglia. These cells are considered the primary immune cell in the CNS but are poorly understood in the context of Toxoplasma. Interactions between astrocytes and microglia and their role in controlling the parasite and immunopathology is a primary focus of the lab.

Activated GFP+ astrocytes following Toxoplasma infection (right: naive; left: infected)

Activated GFP+ astrocytes following Toxoplasma infection (left: naive; right: infected)

T cell recruitment into the CNS following infection

Wilson lab group membersDepletion of CD4+ or CD8+ T cells during infection leads to susceptibility of the host. This is apparent in mouse models and in the human population where Toxoplasma is one of the most serious infections amongst AIDS patients. The recruitment of T cells into the brain is therefore a priority of the immune response. The lab investigates the process by which T cells enter the CNS. Are T cell subsets equally able to migrate into the brain? If not, are the discrepancies due to the type and size of chemokine production or a cell contact mechanism based at the blood brain barrier or are there systems in place within the brain that are important in preventing expansion at the site of infection? In particular collaborations with Dr. David Lo and Dr. Monica Carson at UCR target the role of CCR7 and its ligands during T. gondii infection.

The recently expanding field of live imaging has shown that the movement of cells strongly correlates with their function, thus fast random movement is associated with non-antigen specific interactions and vice versa. Live imaging of Toxoplasma infected brains shows a heterogeneous population of T cells with both fast moving and stationary cells. The lab uses multi-photon microscopy, confocal imaging and gene targeting to address the functional significance of cell motility.

This type of information may more practically lead to immunotherapies that will allow us to control the type, size and longevity of an immune response in the brain.

Tracking GFP+T cells following live imaging in the brain

Tracking GFP+T cells following live imaging in the brain

Selected Publications:

List of publications from PubMed

Lab Personnel:

Nance, J. Philip
Graduate Student Researcher —  Macrophage Response to Toxoplasma in the Brain
Noor, Shahani
Graduate Student Researcher — CCL21 and CCR7 Interactions in T cell Behavior in the Infected Brain

 


More Information

General Campus Information

University of California, Riverside
900 University Ave.
Riverside, CA 92521
Tel: (951) 827-1012

Career OpportunitiesUCR Libraries
Campus StatusDirections to UCR

Genomics Information

Institute of Integrative Genome Biology
2150 Batchelor Hall

Tel: (951) 827-7177
E-mail: Aurelia Espinoza, Managing Director

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