anti-SS-A (Ro) antibody

The epitope recognized by SS-A (Ro) is located on the two proteins (60 x 103 and 52 x 103) which form a complex with the small RNAs hY1, hY3, hY4, hY5. The function of such ribonucleic acid granules is currently unknown, and autoantibodies in the patient's serum may be directed against one of them, or more commonly at the same time for both protein complexes. From the molecular biology point of view, the two proteins and their genes are highly conserved and characteristically repeated, and there is no close relationship between the two. Therefore, antibodies against both proteins are not due to cross-reactivity.

Basic Information

Specialist classification: growth and development check classification: immunological examination

Applicable gender: whether men and women apply fasting: not fasting

Analysis results:

Below normal:

Normal value:

Above normal:

Normal people are negative.

It is suggested that there may be a dry syndrome.

Tips: Because the Ro60 epitope is partially conformational, it is destroyed in immunoblotting. Normal value

Normal people are negative.

Clinical significance

(1) Sjogren's syndrome, SLE According to the sensitivity of the method, the anti-SS-A (Ro) positive rate in patients with primary Sjogren's syndrome can reach 70% to 100%, and in SLE is 24% to 60%. Patients with anti-SS-A-positive SLE often have Sjogren's syndrome or photo-sensitive disease, especially when antibodies are high titers. Anti-SS-B (La) is also usually positive in these cases, and there is evidence that it is often distinguished from primary Sjogren's syndrome, although this is not well understood. Patients with primary Sjogren's syndrome who are anti-SS-A and anti-SS-B positive usually exhibit more in vitro symptoms of the gland, such as vasculitis and lymphadenopathy.

Patients with SLE variants, such as subacute cutaneous lupus (70% to 90%), SLE with complement C2 or C4 deficiency (50% to 90%), have an overall anti-SS-A (Ro) positive rate. Typical SLE patients are high, and in these cases, anti-SS-B (La) is usually undetectable. In 1% of patients with SLE, ANA cannot be detected even during the active period, but anti-SS-A (Ro) can be detected in 60% of such cases.

(2) Neonatal lupus, congenital heart disease anti-SS-A (Ro) and anti-SS-B (La) can be used as prenatal monitoring indicators for pregnant women. Pregnant women or newborns with congenital heart disease or lupus have an anti-SS-A (Ro) positive rate of 100%, and anti-SS-B (La) is also commonly available. These antibodies are considered to be autoimmune through the placenta. A typical example. 5% to 10% of anti-SS-A positive mothers can produce children with these symptoms, such as low anti-SS-A (Ro) titers, anti-SS-B (La) negative, or anti-SS-A immunization This risk is reduced if not detected in the blotting method. During pregnancy and production, most mothers do not meet the diagnostic criteria for SLE or primary Sjogren's syndrome. Many people are even completely asymptomatic. After a certain period of time, most women can progress to SLE with primary symptoms and primary dryness. Sign or connective tissue disease.

(3) Relationship between HLA-DR3 and anti-SS-A (Ro) The genetic background of SS-A (Ro) formation is related to HLA-DR3. Patients with anti-SS-A (Ro)-positive SLE, subacute cutaneous lupus, primary Sjogren's syndrome, congenital heart disease, or neonatal lupus are more likely to have DR3. In the latter two cases, the mother is almost all It is a carrier of DR3, but the child is not necessarily a carrier.

(4) Clinical specificity of anti-SS-A (Ro) The clinical specificity of these diseases is relatively low. Even with the relatively low sensitivity immunodiffusion method, the positive rate of anti-SS-A in healthy women is 0.44%. If the sensitivity is high, this percentage will increase. Unfortunately, anti-SS-A testing does not distinguish between primary or secondary Sjogren's syndrome.


Anti-SS-A (Ro) is often found in ANA-negative SLE patients. Many matrices, especially conventional methanol-fixed Hep-2 cells, do not exhibit anti-SS-A in the form of ANA in the IFT response. This is because the titer is low, some antigens are located in the cytosol or the antigen is washed away during the fixation process. If clinically suspected to be SLE, and ANA is negative, anti-SS-A (Ro) and anti-phospholipid antibodies should be tested.

Although anti-SS-A (Ro) is known to have two different target antigens (Ro52, Ro60), most assays, such as immunodiffusion, reverse phase immunoelectrophoresis, and ELISA established with purified antigens, cannot distinguish them. Western blotting and ELISA using Ro52 and Ro60 recombinant antigens can detect two anti-SS-A (Ro), respectively. According to the statistics of immunoblotting, Ro52 antibody has a stronger relationship with Sjogren's syndrome, while Ro60 antibody is more closely related to SLE. However, since 30% of the Ro positive serum immunoblotting is negative, this conclusion has limitations, especially since the Ro60 epitope is partially conformational and is destroyed in immunoblotting. If a sufficiently sensitive method is used, most of the Ro-positive sera can detect both antibodies.

Inspection process

(1) Precipitation method: Unlike the detection methods similar to anti-Sm, anti-RNP or anti-SS-B, calf, rabbit and thymus extracts cannot be used for immune double-diffusion and reversed-phase immunity because they do not have sufficient concentration of Ro antigen. Electrophoresis, and is mainly obtained from human spleen tissue or human cultured cells (WI-L2). The sedimentation band was identical to the reference serum and verified to be SS-A specific.

(2) Immunoblotting: The antigen is a cell culture such as HeLa or MolT-4. When there are two identical typical bands (60 x 103 and 52 x 102) with the reference serum, it is confirmed to be anti-SSA (Ro) positive.

(3) ELISA: Affinity purified or recombinant 52×103 and 60×103 proteins, or relatively purified hY-RNP particles can be used as antigens.

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Adverse reactions and risks

There are no related complications and hazards.