Inflammation is essential to the immune system's ability to destroy invading infections, damaged cells, and cancers. However, excessive inflammation can be detrimental to the host. To counter this process, the immune system evolved to control anti-inflammatory responses. The equilibrium between pro- and anti-inflammatory immune responses, known as "immune homeostasis," is crucial for the host's health. While immune homeostasis can be disrupted broadly, it can also be localized, as demonstrated in tissue-specific inflammatory disorders like psoriasis and inflammatory bowel disease, emphasizing the importance of immunological homeostasis at the individual tissue level in maintaining health.

The old perspective of how our bodies work, such as how immunological homeostasis is maintained, was that our genes dictate how our bodies function. However, studies have revealed that our microbiota and exposure to environmental stimuli have a substantial impact on our biology. As a result, human biology is now thought to be determined by our genes, microbiota, and environmental exposure.

Dr. Kim's previous work includes a groundbreaking study that identified the processes of T cell homing to the colon for the first time, revealing how local immunological homeostasis is achieved in the colon. Furthermore, Dr. Kim's laboratory recently discovered how our diet (tryptophan) affects immune homeostasis in the colon, and that consuming more tryptophan reduces the risk of colitis in mouse models, paving the way for a non-invasive therapeutic approach to ulcerative colitis (Van et al., 2023, PMC10645889).

Cigarette smoking and dietary tryptophan consumption have been demonstrated to improve ulcerative colitis symptoms. Dr. Kim's laboratory is presently researching the processes underlying these events.

"Leaky gut" has been identified as a possible cause of numerous human disorders. As a result, keeping an intact gut epithelial cell layer is crucial to human health. To complete this duty, intestinal epithelial cells are regularly regenerated and replaced by stem cell proliferation, which increases the risk of cancer development. Dr. Kim's lab recently discovered a novel role for a protein called C10ORF99 in maintaining the delicate balance between the need for continual proliferation of colon epithelial cells and the necessity to limit colorectal cancer formation. 

Eosinophilic Esophagitis (EoE) is a chronic inflammatory illness characterized by eosinophilic infiltration of the esophagus, esophageal dysfunction, and progressive fibrosis. EoE is the leading cause of dysphagia, esophageal perforation, and food impaction. Nonetheless, little is known about how EoE occurs. Dr. Kim’s lab is now investigating the role of T cell homing to the esophagus in mouse models of EoE.