Regulatory T cells (Treg) are a specific cell population crucial for the maintenance of immunological self-tolerance. Their absence or dysfunction can lead to autoimmunity, yet we still do not fully understand the molecular pathways that regulate Treg biology. We found that the NFκB regulator MALT1 is an important novel regulator of Tregs. Mice deficient for MALT1 display diminished numbers of total Tregs. In young Malt1-/- mice Tregs originated from the thymus (nTregs) are totally absent and diminished in the periphery. Interestingly, Treg numbers increase in older mice or under experimentally induced inflammatory conditions in vivo. These Tregs even exceed levels found in the corresponding WT animals. WT and Malt1-/-Tregs were indistinguishable in respect to their suppressive capacity, but Malt1-/-Tregs express higher levels of Toll like receptor (TLR) 2. In line with this, the TLR2 ligand Pam3Cys was able to strongly enhance Treg induction and proliferation of Malt1-/-T cells in vitro. We thus hypothesize a critical supportive role of MALT1 in nTreg development and a suppressive function of MALT1 in iTreg induction during inflammation. This positions MALT1 as a key molecule that both contributes to tolerance in the steady state, while also ensuring immune reactivity when needed.