Rowell syndrome (RS) is a rare disease characterized by the association of systemic lupus erythematosus (SLE) or cutaneous lupus with lesions similar to erythema multiforme and the presence of autoantibodies including ANA, SSA, SSB, or rheumatoid factor.
We selected a core of an antiphospholipid syndrome-like SLE (aPL+ group; positive in the lupus anticoagulant (LA) test and negative for all three of SSA (Ro52 and Ro60) and SSB antibodies) and a Sjögren's syndrome-like SLE (SSA/SSB+ group; positive for all three of SSA (Ro52 and Ro60) and SSB antibodies but negative in the LA test).
Anti-SSA/SSB serum levels were lower in patients attaining lupus low disease activity state at month 6; these associations were stronger for corresponding immune complex levels.
Compared with the healthy controls, the miR-210 expression levels were significantly increased in patients with SLE (P = 0.001) and there was increased significantly expression of miR-210 in SLE with pleuritis (Z = -2.345, P = 0.019) and anti-SSB/La-positive group (Z = -2.076, P = 0.038).
To our knowledge there are no studies assessing anti-Ro/SSA and anti-La/SSB autoantibodies in a large population of childhood-systemic lupus erythematosus (cSLE) patients.
Only 2% reported performing ANA tests at each visit, while 4-5% performed anti-ENA and anti-SSA/SSB antibody tests at each visit for their SLE patients.
Here we demonstrate that in latently infected B cells, EBER1 transcripts interact with the lupus antigen (La) ribonucleoprotein, avoiding cytoplasmic RNA sensors.
The presence of leukopenia, positive for anti-dsDNA antibody and anti-SSB antibody were associated with UBASH3A mRNA levels in SLE patients (all p < 0.05).
High levels of IFN gene expression in ILE and SLE showed significant correlations with the expression of a subset of IgG autoantibodies, including chromatin, dsDNA, dsRNA, U1snRNP, Ro/SSA, La/SSB, topoisomerase I and Scl 70, while low IFN levels were correlated with immunoglobulin (Ig)M autoreactivity.
We previously reported the establishment of a rabbit (Oryctolagus cuniculus) model in which peptide immunization led to production of lupus-like autoantibodies including anti-Sm, -RNP, -SS-A, -SS-B, and -dsDNA characteristic of those produced in systemic lupus erythematosus (SLE) patients.
Using the recombinant La (SS-B) protein or a phosphorylated peptide derived thereof 27 La-specific human recombinant autoantibodies were selected from anti-La-positive systemic lupus erythematosus and systemic sclerosis patient-derived combinatorial phage display antibody libraries.
Human anti-SSB/La autoantibodies purified from active SLE sera passing through the recombinant SSB/La conjugated Sepharose 4B affinity column could bind and penetrate into normal human PMN.
Autoantigen La/SSB is molecular target of humoral autoimmunity in patients with primary Sjogren's Syndrome (pSS) and systemic lupus erythematosus (SLE).
A total of 122 sera with anti-La/SSB activity, from patients with primary Sjögren's syndrome (pSS) or systemic lupus erythematosus (SLE), were tested in various peptide-based assays.
Phage clones selected for the presence of insert both by gene and antigenic analyses were used in the ELISA to detect anti-La/SS-B antibodies from patients with Sjogren's syndrome and SLE.
Because the SS-A/Ro and SS-B/La autoantibody responses in SS and systemic lupus erythematosus (SLE) show even stronger correlations with HLA alleles, HLA-DR and DQ alleles were examined using restriction fragment length polymorphisms (RFLP) in white and black patients with SS and/or SS having anti-Ro and anti-La antibodies.
Frequencies of autoantibodies to Sm, nRNP, Ro (SSA) and La (SSB) were determined by countercurrent immunoelectrophoresis (CIE) and/or enzyme linked immunosorbent assays (ELISA) in 106 whites and 60 blacks with systemic lupus erythematosus.
We measured the prevalence of ANA and antibodies against DNA, RNP, Sm, SSA, and SSB as well as antilymphocyte antibodies (ALA) in the serum of 24 patients with childhood onset SLE and 94 of their first degree relatives and compared the prevalence of these same antibodies in 8 patients with adult onset SLE and 33 of their first degree relatives.