Transcription profiling of mouse interferon-I?-dependent regulatory circuits in immune inflammation highlighted in diabetes

ABSTRACT: We demonstrate diverse roles of interferon–gamma (IFN-γ) in the induction and regulation of immune-mediated inflammation using a transfer model of autoimmune diabetes. The diabetogenic CD4+BDC2.5 (BDC) T cell clone upon transfer into NOD.scid mice induced destruction of islets of Langerhans leading to diabetes. Administration of a neutralizing antibody to IFN-γ (H22) resulted in long term protection (LTP) from diabetes, with inflammation but persistence of a significant, albeit decreased numbers of β-cells. BDC T cells were a mixture of cells expressing high, intermediate and low levels of the T cell receptor. Clonotype-low BDC T cells were required for LTP. Furthermore, islet infiltrating leukocytes in the LTP mice contained Foxp3+CD4 T cells. Islet inflammation in both diabetic and

ORGANISM(S): Mus musculus

SUBMITTER: Jason Mills 

PROVIDER: E-GEOD-12389 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress