U1 snRNPs bind to TLR7 and drive cytokine production by human dendritic cells.
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...
The Rockefeller University Press
2005
The Rockefeller University Press
2005
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