| Summary: | Kawasaki disease (KD) is a childhood vasculitis with a predilection for the coronary arteries (CA). The etiology of KD is unknown; however, superantigens (SAg) have been implicated. SAg-activated T cells undergo massive proliferation followed by apoptosis; conversely, in KD these T cells may persist and target the CAs. Enhanced costimulation can rescue SAg-activated T cells from apoptosis, and Toll-like receptor 2 (TLR2) enhances costimulation. In a murine model of KD, TLR2-deficient mice are disease resistant, and evidence suggests preferential expression of TLR2 at the CA. Results from this study demonstrate that TLR2 is rapidly expressed in the heart following disease induction, and that TLR2 is expressed differentially in various arteries. The aorta, from which the CAs branch off, expressed the highest TLR2 levels. A microvascular endothelial cell line was shown to function as an APC following TLR2 stimulation, supporting the proliferation of SAg-activated T cells and their rescue from apoptosis.
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