Serum Antibodies from Patients with Primary Sjögren’s Syndrome and Systemic Lupus Erythematosus Recognize Multiple Epitopes on the La(SS‐B) Autoantigen Resembling Viral Protein Sequences

Haaheim, Lars R.; Halse, Anne‐Kristine; Kvakestad, R; Stern, Baruch; Normann, O; Jönsson, Roland

doi:10.1046/j.1365-3083.1996.d01-2.x

Cited by 44 publications

(18 citation statements)

References 20 publications

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“…The CMV-induced cell surface expression of the La autoantigen can then lead to the production of anti-La antibodies in genetically susceptible individuals. Another potential mechanism leading to the production of anti-La antibodies is the sequence homology of epitopes in the La protein with CMV antigens (molecular mimicry) [34,35]. The best evidence for this hypothesis is the presence of anti-La antibodies in the sera of patients with SS and SLE that cross-react with epitopes on CMV antigens [35].…”

Section: And Slementioning

confidence: 99%

Cytomegalovirus infection in childhood-onset systemic lupus erythematosus

Rozenblyum¹,

Allen²,

Silverman³

et al. 2013

International Journal of Clinical Rheumatology

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Systemic lupus erythematosus (SLE) is a multisystem disease with significant morbidity and even mortality. Cytomegalovirus (CMV) is a ubiquitous herpesvirus that, similar to SLE, can also lead to significant morbidity and mortality in the immunocompromised host. The relationship between SLE and CMV is complex, with observations suggesting that CMV induces the autoimmunity of SLE in addition to occurring in the immunocompromised host with known SLE. In this article, we first consider CMV infection in the immunocompetent host, and further examine how this infection differs in the patient with SLE. We focus on disease mechanisms, CMV detection and treatment. We review the differences between CMV infection, syndrome and disease, as identifying the correct state will determine the appropriate treatment. We propose guidelines for the screening and management of CMV infection in childhood-onset SLE, and recognize that further study in this population is required to increase our understanding of the interplay between these disease entities.

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Section: And Slementioning

confidence: 99%

Cytomegalovirus infection in childhood-onset systemic lupus erythematosus

Rozenblyum¹,

Allen²,

Silverman³

et al. 2013

International Journal of Clinical Rheumatology

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“…Because they react with such antigens irrespective of species origin, and also human origin, they are conceptually defined as true autoantibodies. However, it is not established that the autologous antigens always account for their production, or whether such antibodies are induced as a consequence of stimulation with heterologous antigens mimicking autologous antigens (molecular mimicry, see for example references [1,2]), or complexes between autologous and heterologous antigens [3][4][5] or by other events that may contribute to, but not as a sole factor account for, increased antibody production, such as polyclonal B cell stimulation [6]. However, true autoantibodies may also be induced by autoimmune B-cells and T-cells, both recognizing determinants on single autoantigens or complexes of different autologous molecules, as indicated for antibodies to dsDNA by the pioneering results of Datta et al [7,8].…”

Section: Introductionmentioning

confidence: 99%

Screening Tests for Antinuclear Antibodies (ANA): Selective Use of Central Nuclear Antigens as a Rational Basis for Screening by ELISA

Olaussen

Rekvig

1999

Journal of Autoimmunity

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“…Among them, the sequences 145-164aa, 289-308aa, 301-320aa, and 349-364aa of La/SSB as well as 169-190aa and 211-232aa of Ro 60 kDa, have been extensively studied, exhibiting high sensitivity and specificity for autoantibody detection. [10][11][12][13] Early serological studies have shown positive associations of pSS with HLA-DR3, DR2, DR5, and DRw53. 14 15 Increased frequency of the haplotype HLA-DRB1*0301-DRB3*0101-DQA1*0501-DQB1*0201 has been found in Caucasoid patients with pSS, DRB1*0405-DRB4*0101-DQA1*0301-DQB1*0401 in Japanese patients, and DRB1*0803-DQA1*0103-DQB1*0601 in Chinese patients.…”

mentioning

confidence: 99%

Clinical, immunological, and immunogenetic aspects of autoantibody production against Ro/SSA, La/SSB and their linear epitopes in primary Sjogren's syndrome (pSS): a European multicentre study

Tzioufas

Waßmuth²,

Dafni³

et al. 2002

Annals of the Rheumatic Diseases

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Objectives: To investigate the clinical and immunogenetic aspects of antibody formation against Ro/SSA and La/SSB as well as their linear B cell epitopes in patients with primary Sjögren's syndrome (pSS) from different European countries. Patients and methods: Ninety patients with pSS from six European centres were studied. Serum samples from all patients were tested in a control laboratory for anti-Ro/SSA and anti-La/SSB autoantibodies by RNA precipitation assay and autoantibodies to the previously reported B cell linear epitopes of Ro 60 kDa (p169-190aa and p211-232aa) and La/SSB (p147-154aa, p291-302aa, p301-318aa, and p349-364aa). DNA from 88 patients was used for the determination of HLA-DRB1, -DQA1, and -DQB1 genotypes. Analysis of the results was performed in the 88 patients who were genotyped and tested also for antipeptide antibodies. Results: Antibodies to B cell epitopes of Ro 60 kDa were detected at a low frequency (range 10-37%). In contrast, B cell epitopes of La/SSB were detected frequently (range 58-86%) among the anti-La/SSB positive sera. Autoantibodies to the La/SSB epitope, p349-364aa, were significantly positively associated with longer disease duration (p<0.05), recurrent or permanent parotid gland enlargement (p<0.005), and a higher proportion of non-exocrine manifestations (p<0.005), compared with patients without autoantibodies. The presence of anti-Ro/SSA and anti-La/SSB autoantibodies was significantly associated with the presence of HLA-DRB1*03 and DQB1*02 (p=0.038 and p=0.034, respectively). This association was even more prominent and extended to HLA-DQA1*0501 when patients were stratified according the presence of autoantibodies to discrete La/SSB B cell epitopes in comparison with autoantibody negative patients (p<0.01). They were found also to be highly associated with the alleles HLA-DQB1*02 and HLA-DQA1*0501 as well as the presence of a shared amino acid motif in the region 59-69aa of DQB1 first domain (p<0.01, respectively). Conclusions: Autoantibodies against La/SSB, binding to four synthetic peptides, derived from the sequence of the La protein were identified with increased frequency in sera of patients with pSS. The formation of autoantibodies against B cell epitope analogues of La/SSB in European patients with pSS may be dependent on the presence of a permissive HLA-DQ heterodimer, most prominently represented by the HLA-DQA1*0501/DQB1*0201 heterodimer, suggesting that a model of HLA restricted presentation of La/SSB peptide determinants is crucial for the autoimmune response against La/SSB.

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Serum Antibodies from Patients with Primary Sjögren’s Syndrome and Systemic Lupus Erythematosus Recognize Multiple Epitopes on the La(SS‐B) Autoantigen Resembling Viral Protein Sequences

Cited by 44 publications

References 20 publications

Cytomegalovirus infection in childhood-onset systemic lupus erythematosus

Cytomegalovirus infection in childhood-onset systemic lupus erythematosus

Screening Tests for Antinuclear Antibodies (ANA): Selective Use of Central Nuclear Antigens as a Rational Basis for Screening by ELISA

Clinical, immunological, and immunogenetic aspects of autoantibody production against Ro/SSA, La/SSB and their linear epitopes in primary Sjogren's syndrome (pSS): a European multicentre study

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