U1 snRNPs bind to TLR7 and drive cytokine production by human dendritic cells.

According to a study on page 1575, cellular debris might help trigger the autoimmune disease systemic lupus erythematosus (SLE). Vollmer and colleagues show that endogenous complexes of RNA and protein, often released from dying cells, engage activating receptors in dendritic cells (DCs). The activated DCs then launch an inappropriate immune response against these self-complexes, thus triggering autoimmune disease.

In patients with SLE, the clearance of apoptotic cells is often delayed, in part because of unexplained defects in macrophage phagocytosis. As a result, cellular debris accumulates and is thought to be a source of autoantigens. But a simple piling up of undisposed waste does not explain the specificity of the autoantibody response in patients with SLE—a response selectively targeted against nucleic acid–containing molecules, including chromatin and small nuclear ribonucleoproteins (snRNPs).Vollmer and colleagues...

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