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Letting “SLE-P”ing plaques lie
Patients with the autoimmune disease systemic lupus erythematosus (SLE) are more likely to develop atherosclerosis than healthy individuals. Smith et al. hypothesized that invariant natural killer T (iNKT) cells contribute to this process because of their connection to both immune responses and lipids. They found that iNKT cells from SLE patients with asymptomatic plaque (SLE-P) produced more of the T helper 2 (TH2) cytokine interleukin-4 than those from SLE patients with no plaques. These SLE-P iNKT cells were associated with changes in lipid composition and monocyte skewing to the M2 phenotype. These data suggest that SLE-P iNKT cells may connect changes in lipids and the immune response, contributing to the development of cardiovascular disease in SLE patients.
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