Bound to arthritis

Gfi-1 also dampens the cells’ tendencies toward the Th17 and T reg cell lineages. Gfi-1 inhibited production of IL-17 and blocked the expression of CD103, which is found on certain T reg cells. In a model of autoimmunity, mice that lacked Gfi-1 developed a preponderance of CD103expressing T reg cells, thus delaying the onset of disease. The protein prevented gene expression by binding to loci in the genes encoding IL-17 and CD103. Gfi-1 binding triggered histone modifications—most likely via its known interaction with the LSD1 histone demethylase—thus turning off gene expression. Gfi-1 expression was repressed by the cytokine TGF , which drives Th17 and T reg cell differentiation, allowing induction of those cells when needed. Examining expression of Gfi-1 in various human infections may help explain why the balance of cell types can sometimes be tipped in the wrong direction.