The Researcher’s Summary:
Physicians and scientists have accepted for a long time the idea that juvenile idiopathic arthritis (JIA) is triggered by complex gene-environment interactions, but we have not been able to characterize how those interactions actually happen. The new field of epigenetics, the study of alterations in DNA that occur as the result of environmental cues but don’t alter the actual genetic code, provides tremendous opportunity to understand these complex interactions.
In this project, we will be examining epigenetic alterations in a specific type of white blood cell in JIA, called a neutrophil. Neutrophils are a cell of the innate immune system, the part of the immune system that does not require prior exposure to a germ or virus for maximum function. We have previously shown that these cells show specific alterations in juvenile arthritis, and this study is intended to understand those alterations in function at the genome level. We will look across the genome at specific epigenetic changes in JIA neutrophils, and examine how those changes affect what genes and gene variants JIA neutrophils use, comparing the results to healthy control children
This project, then, will set the stage for deeper and more complex studies into how the genome functions in JA and an understanding of both the disease and its response to therapy at the genome level.