Anti-SSA/Ro autoantibodies

Clark et al. referred to the antigen as Ro – named after the patient from which the antibodies were extracted,[3][5] while Alspaugh & Tanand used the term SSA.

[3] In laboratory settings, ELISA and immunodiffusion assays are most commonly used to detect levels of Anti-Ro/SSA antibodies in patient sera.

[3][8] Some proposed factors that may stimulate production are viral infection, treatment of cells with TNF-α, cellular apoptosis, and exposure to UV irradiation.

[3] The Ro52 gene is officially termed TRIM21, as it is a member of the tripartite motif protein (TRIM) family, qualified by its RING and B-box domains.

The protein is typically located in the cytoplasm, though it can move to the nucleus in the presence of pro-inflammatory signals, and it can also be expressed on the cell surface.

[7] Ro52 is a regulatory protein, and negatively moderates inflammatory response, such as the secretion of pro-inflammatory cytokines in the interleukin and INF families.

[3] Ro52 may impact the pathogenesis of autoimmune disease: patients with SLE and SS have been shown to express high levels of Ro52 transcripts.

Additionally, Anti-Ro52 antibody has been identified at elevated levels in patients with interstitial lung disease, as well as in autoimmune hepatitis type 1.

Ro60 is encoded by a gene 32 kb in length and acts to regulate the fate of misfolded RNA within the host cell.

The presence of Anti-SSA/Ro in pregnant women with SLE is associated with an increased risk of neonatal lupus erythematosus which can be accompanied by congenital heart block (CHB) in the fetus.

[12] SLE-related symptoms in infants that arise from Anti-Ro/SSA resolve in about six months as the mother's antibodies leave the baby's system.