ArrayExpress Uploaderarrayexpress_sidmouseWTnoneWTnoneWTnoneWTIFNalpha for 90 minutesWTIFNalpha for 90 minutesWTIFNalpha for 90 minutesWTIFNalpha for 90 minutesWTafter 8 days of LCMV infectionWTafter 8 days of LCMV infectionWTafter 8 days of LCMV infectionWTafter 8 days of LCMV infection and treated with IFNalpha for 90 minutesWTafter 8 days of LCMV infection and treated with IFNalpha for 90 minutesWTafter 8 days of LCMV infection and treated with IFNalpha for 90 minutesSTAT1 KOnoneSTAT1 KOnoneSTAT1 KOnoneSTAT1 KOIFNalpha for 90 minutesSTAT1 KOIFNalpha for 90 minutesSTAT1 KOIFNalpha for 90 minutesSTAT4 KOnoneSTAT4 KOnoneSTAT4 KOnoneSTAT4 KOIFNalpha for 90 minutesSTAT4 KOIFNalpha for 90 minutesSTAT4 KOIFNalpha for 90 minutes828607Type 1 IFNs can conditionally activate all of the signal transducers and activators of transcription molecules (STATs), including STAT4....E-GEOD-40666/profile/8773/arrayexpressuploader225cellDec.12, 2014FalseE-GEOD-40666_A-AFFY-23regulating-type-1-ifn-effects-in-cd8-t-cells-durinRegulating type 1 IFN effects in CD8 T cells during viral infections: changing STAT4 and STAT1 expression for functionNov.23, 2014Type 1 IFNs can conditionally activate all of the signal transducers and activators of transcription molecules (STATs), including STAT4. The best-characterized signaling pathways use STAT1, however, and type 1 IFN inhibition of cell proliferation is STAT1 dependent. We report that type 1 IFNs can basally stimulate STAT1- and STAT4- dependent effects in CD8 T cells, but that CD8 T cells responding to infections of mice with lymphocytic choriomenigitis virus have elevated STAT4 and lower STAT1 expression with significant consequences for modifying the effects of type 1 IFN exposure. The phenotype was associated with preferential type 1 IFN activation of STAT4 as compared to STAT1. Stimulation through the TCR induced elevated STAT4 expression, and STAT4 was required for peak expansion of antigen-specific CD8 T cells, low STAT1 levels, and resistance to type 1 IFN-mediated inhibition of proliferation. Thus, a mechanism is discovered for regulating the consequences of type 1 IFN exposure in CD8 T cells, with STAT4 acting as a key molecule in driving optimal antigen-specific responses and overcoming STAT1-dependent inhibition of proliferation. CD8 T cells were purified from uninfected WT, STAT1-deficient and STAT4-deficient mice or from D8 LCMV-infected WT mice and either control treated or treated with 1x104 U mouse IFNalpha for 90 minutes.http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-40666http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-40666/samples/