Microarray expression data from WT and Irf4-/- CD4+ T cells after activation. Mus musculus

To define molecular basis underlying dysfunction of Irf4-deficient T cells. We found that Irf4-deficient T cells were dysfunctional and unable to infiltrate and reject heart allografts, and then investigated the molecular basis underlying dysfunction of Irf4-deficient T cells. Irf4-deficient and wild type B6 CD4+ T cells were activated in vitro for two days, followed by microarray analysis. We found that dysfunction of Irf4-deficient T cells is not only due to impaired effector differentiation, but also involves an altered transcriptional programme that allows the expression of essential negative regulators of T-cell function. Overall design: Naive CD4+ T cells (CD62L+CD44−) were sorted by flow cytometry Irf4-/- and wild type B6 mice, then 1×10e5 cells per well were activated with mAb to CD3e (1 μg/ml; 2C11; Biolegend) plus equal numbers of syngeneic mitomycin C-treated antigen-presenting cells in 96-well round bottom tissue-culture plates at 37 ºC in a humidified incubator with 5% CO2. Two days later, living CD4+ T cells were sorted by Flow Cytometry for RNA isolation. The total RNA samples were then used for microarray analysis. Two independent experiments for WT and Irf4-/- were performed.