Abstract:Background
Ro52/TRIM21 is a major target of autoantigenic responses in Sjögren’s syndrome (SS). Up-regulated epithelial Ro52 expression has been reported at the salivary gland inflammatory lesions of SS patients; however, the factors that drive this effect have not been identified. Ro52 is an E3-ubiquitin ligase that negatively regulates TLR3-mediated inflammation by ubiquitinating and promoting proteasomal degradation of several downstream IRFs, whereas both type-I and type-II interferons (IFN) are considered… Show more
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