Categorizing immune responses as innate or adaptive has been the basis of immunological research for decades. However, evidence that blurs the boundaries and merges the mechanisms of these two arms of the immune system is accumulating. Two Review articles and two Research Highlights in this issue provide examples of mechanisms that seem to bridge both systems.

On page 799, David Rawlings and colleagues describe how antigen receptors on B and T cells use signalling machinery that was originally identified in innate cells to mediate activation of nuclear factor-κB (NF-κB). The common signalling platform that is upstream of NF-κB activation by antigen receptors is known as the CARMA1 signalosome. The authors tell us how the CARMA1 signalosome is assembled and how it promotes the recruitment of components that participate in signalling through innate immune receptors in lymphocytes.

On page 823, Ann Marshak-Rothstein explains how Toll-like receptors (TLRs) might be involved in activating B cells in systemic autoimmune disease. In this regard, TLRs might function not only as innate sensors of microbial molecules but also as sensors of endogenous molecules and directly trigger the production of autoantibodies by autoreactive B cells.

We also highlight a recent report (page 794) in which researchers were surprised to observe that some neutrophils, which typify the immediate innate immune response, express a T-cell-receptor-based variable immunoreceptor, indicating that these cells might use both innate and adaptive mechanisms for pathogen recognition. Finally, another recent report (highlighted on page 795) has shown that induction of a CD4+ T-cell response to the parasite Toxoplasma gondii depends on TLR-mediated recognition and subsequent presentation of the parasite antigen profilin.