Expression data from BATF-deficient Treg cells

FoxP3 is a central regulator of immunological tolerance, controlling the development and function of regulatory T (Treg) cells. To dissect the complex processes orchestrated by FoxP3, we investigated impacts of three autoimmune disease-associated missense FoxP3 mutations in mice. The I363V and R397W mutations were loss-of-function mutations, causing multi-organ inflammation by globally compromising Treg cell physiology. By contrast, the A384T mutation induced a distinctive tissue-restricted inflammation by specifically impairing the ability of Treg cells to compete with pathogenic T cells in certain non-lymphoid tissues. Because BATF expression was down-regulated in A384T Treg cells, we hypothesized that its down-regulation could account for the A384T Treg cell phenotype and addressed whether BATF-deficient Treg cells are phenotypically similar to A384T Treg cells. CD4(+)hCD2(+) Treg cells from FoxP3hCD2.Batf+/+ or -/- mice were subjected to microarray analysis. All cell populations analyzed were generated in triplicates.