Connective Tissue Diseases

Single Analytes

Autoantibodies against

dsDNA | ssDNA | Histones (IgG/IgM) | U1RNPSm  | SS-A/Ro | SS-B/La | Scl-70CENP | Jo-1 | Rib-P

 

dsDNA

Products Article No. No. of tests
Varelisa dsDNA Antibodies 141 96 96 tests
EliA dsDNA 14-5500-01 4x12 tests 

Promotion Material

Product Folder 
EliA dsDNA (pdf)


Antigens

Deoxyribonucleic acid (DNA) as antigen may be either double-stranded (dsDNA) or single-stranded (ssDNA), but only dsDNA antibodies are specific markers. For use in anti-DNA assays, DNA from tissue, from eukaryotic cell, from bacteria or from bacteriophages is used. Circular plasmid DNA is a very suitable choice, because the risk to incorporate single strands is very low.

In the Varelisa and EliA assays the DNA is coated as recombinant plasmid double-stranded DNA.

Disease association, antibody prevalence and specificity

Systemic lupus erythematosus (SLE), dependent on method used and on the activity status of patients the antibody prevalence varies betwenn less than 30 to more than 90%.  Anti-dsDNA antibodies belong to the ARA diagnostic criteria for SLE.

To learn more:


The disease specificity varies highly, dependent on the method used. With highly sensitive methods, anti-dsDNA can be found in uveitis, discoid lupus erythematosus, rheumatoid arthritis, juvenile rheumatoid arthritis and further in a wide variety of patients. In these cases, we are mostly dealing with antibodies of the IgM isotype of IgG with low avidity.  

Disease activity

Good correlation of anti-dsDNA titer and disease activity, thus important for monitoring, especially high aviditiy IgG antibodies. A rise of the antibody titer can predict an exacerbation of the disease. Quantitative anti-dsDNA IgG should be measured regularly in SLE patients.

When is the measurement recommended?

Suspicion of SLE, monitoring of SLE.

Antibody isotypes

IgG. IgM is often determined, but the clinical significance in diagnosis and monitoring is reduced.

Detection methods

IIf on Crithidia luciliae (CLIFT), radiobinding assays (mainly Farr assay) and enzyme-linked immunosorbent assays (ELISA).

References

  • Hochberg MC (1997) Updating the American College of Rheumatology Revised Criteria for the Classification of Systemic Lupus Erythematosus. Arthr Rheum 40, 1725-1734
  • Bootsma H, Spronk PE, Ter Borg EJ et al. (1997) The predictive value of fluctuations in IgM and IgG class anti-dsDNA antibodies for relapses in systemic lupus erythematosus. A prospective long term observation. Ann Rheum Dis 56, 661-666 
  • Tzioufas AG, Tergoglou C, Stavropoulos ED et al. (1990) Determination of anti-dsDNA antibodies by three different methods: Comparison of sensitivity, specificity and correlation with lupus acticity index (LAI). Clin Rheumatol 9, 186-192

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ssDNA

Product Article No. No. of tests
Varelisa ssDNA Antibodies 148 96 96 tests

Antigen

In 1971 Cohen et al. proposed three categories of antibodies directed against the DNAmolecule:

  • The first category is directed against conformational epitopes associated with the native doublehelical structure. By definition these DNA antibodies are the only true dsDNA antibodies. However, they seem to be rare.
  • The second group targets the polymers of purine and pyrimidine bases, which as antigens are accessible to the immunocompetent cells only in the singlestranded DNA, i.e. in the denatured state. These antibodies are considered the only true ssDNA antibodies.  
  • The third group targets the desoxyribose-phosphate backbone, which is equally present in ssDNA and dsDNA molecules. Accordingly they are neither true dsDNA nor ssDNA antibodies. The majority (85 to 95%) of DNA antibodies in patient samples belongs to this category.

From a technical point of view it is impossible to measure in a single test true ssDNA antibodies (with purine and pyrimidine bases being the sole antigen). All ssDNA antibodies tests measure DNA antibodies belonging to category 2 and 3. ssDNA antibodies are commonly found in SLE and drug-induced lupus (DIL). Together with histone antibodies and in the absence of dsDNA antibodies they may be an aid in the diagnosis of DIL. However, they are not specific but occur also in systemic and localized scleroderma, liver disorders, a number of connective tissue diseases and some normal individuals.

In the Varelisa assay the plate is coated with synthetic single stranded DNA.

When is the measurement recommended?

Suspicion of SLE or drug-induced lupus.

Antibody isotypes

IgG

Detection methods

Enzyme-linked immunosorbent assays (ELISA).

References

  • Takehara K et al. Anti-Single-Stranded DNA Antibody and Muscle Involvement in Localized Scleroderma. Arch Dermatol 1990; 126:1368-1369
  • Ruffati A et al. Prevalence and Characteristics of Anti-Single-Stranded DNA Antibodies in Locolized Scleroderma.
  • Lange A. Evaluation of the simultaneous estimation of anti-dsDNA and anti-ssDNA antibodies for clinical purposes. Clin Exp Immunol 1978; 31:472-481

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Histones

Product Article No. No. of tests
Varelisa Histone (IgG/IgM) Antibodies 164 96 96 tests

Antigen

As an autoimmune disease SLE is characterized by a complex clinical picture and by a great diversity of autoantibodies. Antibodies against dsDNA and RNP-Sm are the most prominent ones in the diagnosis of SLE since they demonstrate high specificity for the disease. Of comparable prevalence are antibodies against DNA binding histone proteins (H1, H2A/H2B, H3 and H4). They can be found in up to 50 % of all SLE patient sera. Their frequency increases to 80 % in patients with the acute disease. Anti Histone Antibodies (AHA) are of clinical importance for the diagnosis of drug-induced lupus erythematosus. Drugs such as hydralazine, procainamide and isoniazide are known for their LE inducing effect. In addition to antibodies against single histones, antibodies against histone complexes such as H2A-H2B and H3-H4 are frequently found in DIL. Dependent on the inducing drug, up to 90-95 % of DIL patients are positive for histone autoantibodies. However, the test is of limited value as these antibodies are found in other diseases such as infections. AHA have also been found in patients with rheumatoid arthritis, mixed connective tissue disease and progressive scleroderma. The incidence of AHA in these patients however is low ranging from 10 to 15 percent.

In the Varelisa assay the plate is coated with purified human histone proteins H1, H2A, H2B, H3 and H4.

When is the measurement recommended?

Suspicion of drug-induced lupus. 

Antibody isotypes

IgG and IgM (measured with mixed conjugate)

Detection methods

Enzyme-linked immunosorbent assays (ELISA).

References

  • Rubin R. Histone (H2A-H2B)-DNA Autoantibodies. In: Peter JB, Shoenfeld Y (eds) Autoantibodies. 1996; pp 364-372. Elsevier, Amsterdam
  • Harmon CE, Portanova JP. Drug-induced lupus erythematosus. Clin Rheum Dis 1982; 8:121-135
  • Shoenfeld Y, Segol O. Anti-histone antibodies in SLE and other autoimmune diseases. Clin Exp Rheumatol 1989; 7:265-271

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 U1RNP

Products Article No. No. of tests
Varelisa RNP Antibodies 170 96 96 tests
Varelisa RNP-Sm Antibodies 165 96 96 tests
EliA U1RNP 14-5501-01 4x12 tests
EliA RNP70 14-5511-01 4x12 tests

Promotion Material

Performance Folder
EliA ANA Differentiation (pdf)
Sm, U1RNP, RNP70, Ro, La, Scl-70, CENP, Jo-1

Antigens

In their natural state, the small nuclear RNAs, also called U-RNAs (for "uracil rich RNAs"), exist as ribonucleoprotein particles (snRNP). The U1 snRNA is present as complex with the Sm proteins, which are found also in the U2, U4 and U5 snRNPs, and the U1-specific proteins 70 kDa, A (34 kDa) and C (22 kDa).

U1 snRNP complexes are primarily localized in the nucleoplasm and are involved in the splicing process.

The Varelisa RNP Antibodies assay and the EliA U1RNP and RNP Wells use human recombinant U1 snRNP proteins. The Varelisa RNP-Sm Antibodies assay contains the purified complex.

Disease association, antibody prevalence and specificity

  • Systemic lupus erythematosus (SLE) (30-40%) anti-RNP may occur alone but often present in conjunction with other specificities. Anti-Sm positive sera are almost always also positive for anti-RNP.
     
  • Mixed connective tissue disease (MCTD) is defined by the presence of high titer anti-RNP (especially anti-70 kDa antibodies, but also anti-A and -C).
     
  • Anti-U1 RNP antibodies may also occur in a small fraction of patients with Sjögren's syndrome, rheumatoid arthritis, scleroderma, and polymyositis.

Disease activity

Longitudinal studies have indicated that anti-U1 RNP antibody titers vary over time, but it is uncertain whether these levels reflect underlying disease activity.

When is the measurement recommended?

Suspicion of SLE or MCTD.

Antibody isotype

IgG

Other detection methods

IIF on HEp-2 (coarse speckled pattern). The immunofluorescence technique cannot distinguish between anti-U1 snRNP and anti-Sm antibodies. Other techniques (immunodiffusion, immunoblotting, RNA immunoprecipitation etc.) are possible but not necessarily useful for routine.

References

  • Van den Hoogen FHJ, Van de Putte LBA (1996) ANti-U1snRNP antibodies and clinical associations. In: Van Venrooij WJ, Maini RN (eds.) Manual of Biological Markers of Disease, Kluwer Academic Publishers, Amsterdam 
  • Craft J, Hardin J (1992) Anti-snRNP antibodies. In: Wallace DJ, Hahn BH (eds.), Dubois' Lupus Erythematosus, pp 216-219, Williams and Wilkens 
  • Peng SL, Craft JE (1996) Spliceosomal snRNPs autoantibodies. In: Peter JB, Shoenfeld Y (eds.), Autoantibodies, pp 774-782, Elsevier Science B.V., Amsterdam

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Sm

Products Article No. No. of tests
Varelisa Sm Antibodies 182 96 96 tests
EliA Sm 14-5502-01 4x12 tests

Promotion Material

Performance Folder
EliA ANA Differentiation (pdf)
Sm, U1RNP, RNP70, Ro, La, Scl-70, CENP, Jo-1

Antigens

In their natural state, the small nuclear RNAs, also called U-RNAs (for "uracil rich RNAs"), exist as ribonucleoprotein particles (snRNP). The U snRNP U1, U2, U4, U5 and U6 all contain a group of proteins, the so-called Sm peptides, with the major targets being the B and D polypeptides. Because of cross-reactivity between the A, the C and the B/B' proteins, up to 60% of anti-U1 RNP sera may react with B/B'. Thus, only the presence of anti-D and/or the absence of anti-A and anti-C can be regarded as characteristic for an anti-Sm sera. Until now, all trials to produce an antigenic recombinant SmD protein with a good reactivity failed because of its very special structure. In 2004, an ELISA using a dimethylated SmD peptide was developed which showed to have a significantly higher specificity than traditional assays with purified SmD.

EliA Sm Well is coated with a purified Sm antigen. Varelisa Sm Antibodies assay is coated with SmD peptide.

Disease association, antibody prevalence and specificity

Systemic lupus erythematosus (SLE) (10-20% in caucasian SLE patients), Sm antibodies are highly specific, but relatively insensitive marker for SLE. Their presence constitutes one of the revised ARA criteria for diagnosis.

To learn more:


Anti-Sm positive sera are almost always also positive for anti-RNP.

Anti-Sm reactivity is not described definitely in other diseases, although a few studies describe Sm antibodies in monoclonal gammopathies, schizophrenia and uveitis.

Disease activity

Numerous studies suggest the association of anti-Sm antibodies with disease activity and particular disease manifestations.

When is the measurement recommended?

Suspicion of SLE.

Antibody isotype

IgG

Other detection methods

IIF on HEp-2 (punctate staining pattern throughout the nucleus; only the nucleolar regions are generally unstained). The immunofluorescence technique cannot distinguish between anti-U1 snRNP and anti-Sm antibodies. Other methods (e.g. counterimmunoelectrophoresis, immunoprecipitation; immunoblotting) can be used but are not necessarily useful for routine.

References

  • Mahler M, Fritzler MJ, Blüthner M (2004) Identification of a SmD3 epitope with a single symmetrical dimethylation of an arginine residue as a specific target of a subpopulation of anti-Sm antibodies. Available online http://arthritis-research.com/content/7/1/R19
  • Peng SL, Craft JE (1996) Spliceosomal snRNPs autoantibodies. In: Peter JB, Shoenfeld Y (eds.), Autoantibodies, pp 774-782, Elsevier Science B.V., Amsterdam 
  • Hoch SO (1994) Autoantigens in SLE - Sm. In: Van Venrooij WJ, Maini RN (eds.) Manual of Biological Markers of Disease, Kluwer Academic Publishers, Amsterdam 
  • Craft J, Hardin J (1992) Anti-snRNP Antibodies. In: Wallace DJ, Hahn BH (eds.) Dubois' Lupus erythematosus. Lippincott Williams & Wilkins

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SS-A/Ro

Products Article No. No. of tests
Varelisa SS-A/Ro Antibodies 166 96 96 tests
EliA Ro 14-5503-01 4x12 tests

Promotion Material

Performance Folder
EliA ANA Differentiation (pdf)
Sm, U1RNP, RNP70, RO, La, Scl-70, CENP, Jo-1


Antigens

The SS-A/Ro particle contains a hY RNA (human cytoplasmic RNA) and associated proteins: a 60 kDa and a 52 kDa protein. The 52 kDa protein is not directly bound to the hY RNA but to the 60 kDa protein. It seems that it is sometimes associated, sometimes not. The Ro antigen is found in the cytoplasm but also in the nucleus. The role of the SS-A/Ro particle in the cell is not known yet.

Phadia assays use human recombinant Ro 60 and Ro 52.

Disease association, antibody prevalence and specificity

  • Primary Sjögren's syndrome (60-75%), part of the diagnostic criteria 
  • Secondary Sjögren's syndrome (about 80%) 
  • Systemic lupus erythematosus, SLE (40-50%) 
  • Mothers of children with neonatal lupus syndrome (100%), but only one in 50 children born to mothers with anti-Ro develop heart block. 
  • Rheumatoid arthritis (2-10%) 
  • Other autoimmune diseases (rarely, with sensitive methods) 
  • Normal controls (0.5%)

Anti-Ro 52 kDa are frequently found in Sjögren's syndrome, whereas anti-Ro 60 kDa are observed more often in SLE.

To learn more:

Disease activity

Anti-Ro are reflecting the extension of the disease in Sjögren's syndrome and are associated in particular with the extraglandular manifestations and serologic findings of the syndrome. On the other hand, anti-Ro levels do not noticeably fluctuate with disease activity or with steroids and/or immunotherapy.

In SLE patients Ro60, Ro52 and La antibody profile is fixed at an early stage of disease and in most patients hardly changes.

When is the measurement recommended?

  • Suspicion of primary Sjögren's syndrome
  • Skin involvement compatible with subacute cutaneous lupus erythematosus
  • Rheumatoid arthritis, prior to D-penicillamine administration
  • Women with Sjögren's syndrome, SLE or rheumatoid arthritis before and during pregnancy

Antibody isotype

IgG

References

  • Reichlin M, Scofield RH (1996) SS-A (Ro) Autoantibodies. In: Peter JB, Shoenfeld Y (eds.), Autoantibodies, pp 783-788, Elsevier Science B.V., Amsterdam 
  • Mavragani CP, Tzioufas AG, Moutsopoulos HM (2000) Sjögren's syndrome: Autoantibodies to cellular antigens - Clinical and molecular aspects. Int Arch Allergy Immunol 123, 46-57 
  • Scofield RH, Farris AD, Horsfall AC, Harley JB (1999) Fine specificity of the autoimmune response to the Ro/SSA and La/SSB ribonucleoproteins. Arthritis Rheum 42, 199-209

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SS-B/La  

Products Article No. No. of tests
Varelisa SS-B/La Antibodies 166 96 96 tests
EliA La 14-5504-01 4x12 tests

Promotion Material

Performance Folder
EliA ANA Differentiation (pdf)
Sm, U1RNP, RNP70, RO, La, Scl-70, CENP, Jo-1


Antigens

The La/SS-B is a ubiquitously expressed phosphoprotein with 47 kDa, that associates with a variety of small RNAs including the hY RNA of the SS-A/Ro particle. La probably is a transcription termination factor for RNA polymerase III and is found in the cytoplasm as well as in the nucleus.

Phadia assays make use of human, recombinant La.

Disease association, antibody prevalence and specificity

  • Primary Sjögren's syndrome (up to 90%), diagnostic criterion
  • Secondary Sjögren's syndrome (about 50%)
  • Systemic lupus erythematosus, SLE (6-15%)
  • Subacute cutaneous lupus erythematosus (25-35%)
  • Mothers of children with neonatal lupus syndrome (90%)

To learn more:

Anti-La are almost always associated with anti-Ro and particularly the 52 kDa component.

Disease activity

Whether the titer of anti-La correlates with disease activity in Sjögren's syndrome or SLE is unknown. Detection per se of anti-La precipitins is a stable serological finding, which does not fluctuate during the course of disease.

When is the measurement recommended?

  • Suspicion of primary Sjögren's syndrome
  • Skin involvement compatible with subacute cutaneous lupus erythematosus
  • Rheumatoid arthritis, prior to D-penicillamine administration
  • Women with Sjögren's syndrome, SLE or rheumatoid arthritis before and during pregnancy

Antibody isotypes

IgG

References

  • Keech CL, McCluskey J, Gordon TP (1996) SS-B (La) Autoantibodies. In: Peter JB, Shoenfeld Y (eds.), Autoantibodies, pp 789-797, Elsevier Science B.V., Amsterdam 
  • Mavragani CP, Tzioufas AG, Moutsopoulos HM (2000) Sjögren's syndrome: Autoantibodies to cellular antigens - Clinical and molecular aspects. Int Arch Allergy Immunol 123: 46-57 
  • Scofield RH, Farris AD, Horsfall AC, Harley JB (1999) Fine specificity of the autoimmune response to the Ro/SSA and La/SSB ribonucleoproteins. Arthritis Rheum 42: 199-209

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Scl-70 / DNA topoisomerase I

Products Article No. No. of tests
Varelisa Scl-70 Antibodies 169 96 96 tests
EliA Scl-70 14-5506-01 2x12 tests

Promotion Material

Performance Folder
EliA ANA Differentiation (pdf)
Sm, U1RNP, RNP70, Ro, La, Scl-70, CENP, Jo-1 

Antigens

In 1979 antibodies of scleroderma patients where described, which react with a 70 kDa protein. Thus, the antigen was named Scl-70. In 1986, Scl-70 was identified as topoisomerase I (topo-I). Topoisomerase I catalyzes the breaking/rejoining of single-stranded DNA and relaxes supercoiled DNA in vitro. The native enzyme is larger than 70 kDa (100 kDa) but often only its smaller proteolytic fragment is found.

The Varelisa Scl-70 Antibodies assay and the EliA Scl-70 Wells are coated with a human, recombinant Topoisomerase I antigen.

Disease association, antibody prevalence and specificity

  • Scleroderma (30-60%), highly specific 
  • Anti-Scl-70 do not exclude additional AI disorders like SLE, Sjögren's syndrome etc. 
  • Not present in relatives of scleroderma patients or other healthy individuals 
  • Rarely found in Raynaud's syndrome, but than often as predictor of scleroderma

To learn more:

Anti-Scl-70 are rarely found in the same patients as anti-centromere antibodies.

Disease activity

Most studies found, that titer does not correlate with disease activity or duration. However, there is evidence, that anti-Scl-70 levels correlate with disease severity and activitiy in systemic sclerosis (see reference Hu et al., 2003).

When is the measurement recommended?

Suspicion of scleroderm.

Antibody isotypes

IgG

References

  • Vazquez-Abad D, Rothfield NF (1996) Topoisomerase-I (Scl-70) autoantibodies. In: Peter JB, Shoenfeld Y (eds.), Autoantibodies, pp 830-835, Elsevier Science B.V., Amsterdam 
  • Verheijen R (1996) DNA topoisomerase I. In: Van Venrooij WJ, Maini RN (eds.) Manual of Biological Markers of Disease, Kluwer Academic Publishers, Amsterdam 
  • Spencer-Green G, Alter D, Welch HG (1997) Test performance in systemic sclerosis: Anti-centromere and anti-Scl-70 antibodies. Am J Med 103, 242-248 
  • Hu PQ, Fertig N, Medsger TA, Wright TM (2003) Correlation of Serum Anti-DNA Topoisomerase I Antibody Levels With  Disease Severity and Activity in Systemic Sclerosis. Arthritis Rheum 48, 1363-1373

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Centromere Protein (CENP)

Products Article No. No. of tests
Varelisa CENP Antibodies 168 96 96 tests
EliA CENP 14-5505-01 2x12 tests

Promotion Material

Performance Folder
EliA ANA Differentiation (pdf)
Sm, U1RNP, RNP70, Ro, La, Scl-70, CENP, Jo-1


Antigens

The centromere is the primary constriction site of eukaryotic chromosomes where sister chromatids appear most tightly paired. The three main centromere antigens are CENP-A (19 kDa), CENP-B (80 kDa) and CENP-C (140 kDa) but the most important centromere antigen is the CENP-B. Antibodies to CENP-A and -C are usually cross-reacting and are found almost always in combination with anti-CENP-B antibodies. CENP-B is recognized by virtually all sera with anti-centromere antibodies (ACA).

CENP-B is located within the heterochromatin underneath the kinetochore and probably forms a dimer that binds DNA and has an important role in regulating higher order chromatin structure within the centromere.

The Varelisa CENP Antibodies assay and the EliA CENP Well are coated with human recombinant CENP-B.

Disease association, antibody prevalence and specificity

  • CREST (about 55%)  
  • Raynaud's disease (10-15%)  
  • Diffuse systemic scleroderma (very rarely - ACA in SSc indicate a significantly better prognosis)  
  • Other rheumatic conditions with Raynaud's phenomenon, e.g. rheumatoid arthritis, Sjögren's syndrome etc. (33%)  
  • Primary biliary cirrhosis (PBC) (10-20%) 
  • Not found in healthy individuals, even in low titers (or extremely rare)
ACA are rarely found in the same patients as anti-Scl-70
To learn more:

Disease activity

The titer does not correlate with disease activity or duration.

When is the measurement recommended?

Raynaud's syndrome, suspicion or diagnosis of scleroderma, primary biliary cirrhosis.

Antibody isotype

IgG

References

  • McHugh NJ (1996) Centromere autoantibodies. In: JB Peter, Y Shoenfeld (eds.), Autoantibodies, pp. 161-167, Elsevier Science B.V. 
  • Rothfield NF (1996) Autoantibodies to scleroderma-associated antigens. In: Van Venrooij WJ, Maini RN (eds.), Manual of Biological Markers of Disease, Kluwer Academic Publishers, Amsterdam 
  • Spencer-Green G, Alter D, Welch HG (1997) Test performance in systemic sclerosis: Anti-centromere and anti-Scl-70 antibodies. Am J Med 103, 242-248

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Jo-1 / Histidyl-tRNA-Synthetase 

Products Article No. No. of tests
Varelisa Jo-1 Antibodies 167 96 96 tests
Elia Jo-1 14-5507-01 2x12 tests

Promotion Material

Performance Folder
EliA ANA Differentiation (pdf)
Sm, U1RNP, RNP70, RO, La, Scl-70, CENP, Jo-1

Antigens

Jo-1 is synonymous with histidyl tRNA synthetase. This cytoplasmic enzyme catalyzes the eterification of histidine to its cognate tRNA. Binding of anti-Jo-1 antibodies is localized to the cytoplasm of the various cell types examined. Histidyl tRNA synthetase is persent as a homodimer within the cell; identical subunits of approximately 50 kDa are each bound to tRNA. Anti-Jo-1 sera do not recognize other aminoacyl-tRNA synthetases and only histidyl-tRNA synthetases from higher eukaryotes and react with greatest affinity with human enzyme.

The Varelisa Jo-1 Antibodies assay and the EliA Jo-1 Well are coated with human recombinant Jo-1.

Disease association, antibody prevalence and specificity

  • Adult myositis (about 30%) - almost exclusively in patients with myositis: 54% primary myositis, 40% dermatomyositis, 6% myositis in the setting of another connective tissue disease. Patients with anti-Jo-1 tend to have a severe disease with a tendency to relapse and a poorer prognosis. "Anti-synthetase syndrome" is defined by antibodies to anti-tRNA synthetase.
  • Anti-Jo-1 not in myositis: interstitial lung disease (very rarely)

Disease activity

The antibody usually remains detectable throughout the course of disease, and indefinitely thereafter despite control of disease activity. Occasionally, the antibody becomes undetectable, and in those cases it was assocaited with remission of disease. The clinical utility of anti-Jo-1 antibody fluctuation requires further investigation.

Although it would be extremely unusual for anti-Jo-1 antibodies to develop in a patient who was previously negative for the antibody, repeat testing of such a patient might be considered in order to confirm the accuracy of the previous result in a suggestive clinical situation, such as myositis with interstitial lung disease. In a patient found to be positive, besides confirmatory testing if question exist, repeat testing might be considered as treatment is being discontinued, since the risk of reexacerbation is high if the antibody persists.

When is the measurement recommended?

Suspicion of any kind of myositis.

Antibody isotype

IgG

References

  • Maddison PJ (1996) Aminoacyl-tRNA histidyl (Jo-1) synthetases autoantibodies. In: Peter JB, Shoenfeld Y (eds.), Autoantibodies, pp. 31-35, Elsevier Science B.V, Amsterdam
  • Targoff IN, Plotz PH (1996) The autoantibody system: Anti-aminoacyl-tRNA synthetase antibodies. In: Van Venrooij WJ, Maini RN (eds.), Manual of Biological Markers of Disease, Kluwer Academic Publishers, Amsterdam
  • Delarue M (1995) Aminoacyl-tRNA synthetases. Curr Opini Struct Biol 5, 48-55
  • Targoff IN (1992) Autoantibodies in polymyositis. Rheum Dis Clin North Am 18, 455-482

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Ribosomal P

Product Article No. No. of tests
EliA Rib-P 14-5521-01 2 x 12 tests

Antigen

Systemic lupus erythematosus (SLE) is an autoimmune disorder characterized with multiple organ involvement resulting in diability and increased mortality. Antibodies against ribsosomal-P (anti Rib-P) react against acidic phosphorylated ribosomal proteins P0, P1, and P2 (with molecular mass of 38, 19, and 17 kDa, respectively) and are located on the S60 subunit of ribosomes. Anti Rib-P can be detected in approx. 15 to 20% of patients with SLE. They appear highly specific for SLE; therefore, they can be used as diagnostic marker for the disease. Furthermore, association has been described with particular manifestations of lupus, especially with neuropsychiatric, renal, and hepatic involvements. However, results are conflicting regarding the existence of such associations, depending on different study set-up, different study population or different sensitivity of tests used for the detection of anti Rib-P.

The EliA Rib-P Wells are coated with human recombinant ribosomal P-proteins (P0, P1, P2).

When is the measurement recommended?

Suspicion of SLE.

Antibody isotypes

IgG

Detection methods

EliA on Phadia Laboratory Instruments

References

  • Kiss E, Shoenfeld Y. Are Anti-Ribosomal P protein Antibodies Relevant in Systemic Lupus Erythematosus? Clin Rev Allergy Immunol 2007; 32:37-46
  • Gerli L, Caponi L. Anti-ribosomal P protein antibodies. Autoimmunity 2005; 38:85-92
  • Mahler M et al. International Multicenter Evaluation of Autoantibodies to Ribosomal P Proteins. Clin Vaccine Immunol 2006; 13:77-83

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