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Assistant Professor
  • 765-494-1254
  • HANS 309


The immune system is comprised of a variety of cell types that work in a highly organized fashion to protect the body from infection and minimize tumor formation. This organizational process is largely carried out by the adaptive immune system with CD4 + T helper (Th) cells acting to trigger inflammation during infection and also suppress unwanted immune responses to non-harmful stimuli (i.e. allergens, food or normal body microflora). The dual nature (i.e. activator and suppressor) of Th cells is possible due to their unique ability to sense the environment and change their function based on these environmental cues.

Autoimmune disease occurs when the balance between the inflammatory and regulatory functions of Th cells is disrupted, resulting in excess inflammation that alters physiological processes. Inflammatory bowel disease (IBD) and graft-versus-host disease (GVHD) are two forms of intestinal autoimmune disease and are characterized by the accumulation of highly reactive inflammatory T cells in the intestines. However, the exact mechanisms by which inflammatory Th cells arise during inflammation and cause disease are unclear.

In the Olson lab, our goal is to better understand how CD4 + T helper cells drive intestinal inflammation by addressing these key questions:

1) What signals drive the generation of pathogenic/inflammatory Th cells in the intestines?

2) How do pathogenic/inflammatory T helper cells contribute to disease?

3) Can we therapeutically target factors that drive the generation of pathogenic T helper cells or their functional byproducts to eliminate or reduce disease?

My laboratory uses a combination of cell and molecular biology approaches to examine signaling pathways associated with T helper cell differentiation. We also utilize pre-clinical models of disease, and high throughput culturing and RNA/protein profiling techniques to identify disease mechanisms and novel mediators of inflammation.

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