JIA Pathogenesis Related to Neutrophils and Epigenetics Save

Neutrophils are pivotal players in the innate immune response, but are seldom linked to the pathogenesis of inflammatory arthritis, including juvenile idiopathic inflammatory arthritis (JIA).  Jarvis and coworkers from the University of Buffalo sequenced neutrophil RNA from 16 children with the polyarticular, rheumatoid factor–negative form of JIA. They sought to find "gene control switches" that influence both neutrophil and CD4+T cell activities. (Citation source: http://buff.ly/1Kd4ATH)

They identified gene sequences that were strongly associated with polyarticular JIA - H3K4me1 and/or H3K27ac. These regions are also commonly influenced by epigenetic factors. The also identified ncRNA transcripts at the rs4705862 and rs6894249 loci in human neutrophils.

The author concluded that the genetic risk for JIA lies within or adjacent to regions of neutrophil and CD4+ T cell genomes that carry epigenetic marks associated with enhancer function and/or ncRNA transcripts. These findings are consistent with the hypothesis that JIA is fundamentally a disorder of gene regulation that includes both the innate and the adaptive immune system.