Deficiency of Id3 (inhibitor of DNA binding 3) results in Inflammation in salivary glands and gamma-delta (gd) T cell lymphoma (71.11)

Abstract

Abstract Id3-/- mice have been shown to develop a T cell-dependent autoimmune-like sjogren’s syndrome(SS). The dysregulated differentiation between Foxp3+ Tregs and Th17+ T cells in Id3-/- CD4+ T cells promoted us to study whether the autoimmune-like SS in Id3-/- mice was associated with the abnormal expression of Th17 cells in the target organs. We focused on the salivary glands and lachrymal glands, as they are main target tissues involving in SS. 50% of Id3-/- started to show proinflammatory CD4+ infiltrating cells in the salivary glands. Significantly higher frequency of Th1 and Th17 cells were observed in Id3-/- salivary glands, and higher frequency of Th17 and lower frequency of Tregs were observed in Id3-/- spleen. Notably, 26% mice Id3-/- mice developed gd T cell lymphoma. The gd T lymphoma cells were characterized by dysregulated IL-17 production and high expression of an oncogene, c-myc. Adoptive transfer of Id3-/- gd T lymphoma cells to Rag1-/- mice resulted in gd T lymphoma, suggesting that Id3 may regulates gd T cell tumor development.