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A B cell apotope of Ro 60 in systemic lupus erythematosus.
Arthritis Rheum. 2008 Apr; 58(4):1125-9.AR

Abstract

OBJECTIVE

Previous studies have attempted to segregate anti-60-kd Ro/SSA (anti-Ro 60) responses in systemic lupus erythematosus (SLE) and primary Sjögren's syndrome (SS) but have shown limited disease preference. The aim of the present study was to determine whether the presence of autoantibodies against an Ro 60 apotope (an epitope expressed on apoptotic cells) distinguishes anti-Ro 60 responses in SLE and primary SS.

METHODS

Multiparameter flow cytometry was used to select early apoptotic cells and measure the simultaneous binding of annexin V, propidium iodide, and anti-Ro 60-positive IgG from SLE patients (n=21) and patients with primary SS (n=19). The specificity of the Ro 60 apotope was determined by inhibition experiments with recombinant and native Ro 60.

RESULTS

Autoantibodies against the Ro 60 apotope were prevalent in SLE patients (13 of 21, 62%) and were rarely observed in patients with primary SS (1 of 19, 5%) (P=0.0002). Further, within SLE patients, autoantibodies to the Ro 60 apotope strongly distinguished patients with anti-Ro 60 alone (12 of 13, 92%) from those with both anti-Ro 60 and anti-La (1 of 8, 13%) (P=0.0005). When we considered all patients with anti-Ro 60 alone, the presence of autoantibodies to the Ro 60 apotope had both high sensitivity (92.3%) and high specificity (85.7%) for SLE compared with primary SS (P=0.0012). The presence of autoantibodies to the Ro 60 apotope may therefore be of diagnostic value in patients with isolated anti-Ro 60 responses.

CONCLUSION

The preferential targeting of an Ro 60 apotope exposed on early apoptotic cells in a subset of SLE patients implies disease-specific pathways for the induction of anti-Ro 60 autoimmunity.

Authors+Show Affiliations

Department of Immunology, Allergy and Arthritis, Flinders Medical Centre, Bedford Park, South Australia, Australia.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18383373

Citation

Reed, Joanne H., et al. "A B Cell Apotope of Ro 60 in Systemic Lupus Erythematosus." Arthritis and Rheumatism, vol. 58, no. 4, 2008, pp. 1125-9.
Reed JH, Jackson MW, Gordon TP. A B cell apotope of Ro 60 in systemic lupus erythematosus. Arthritis Rheum. 2008;58(4):1125-9.
Reed, J. H., Jackson, M. W., & Gordon, T. P. (2008). A B cell apotope of Ro 60 in systemic lupus erythematosus. Arthritis and Rheumatism, 58(4), 1125-9. https://doi.org/10.1002/art.23377
Reed JH, Jackson MW, Gordon TP. A B Cell Apotope of Ro 60 in Systemic Lupus Erythematosus. Arthritis Rheum. 2008;58(4):1125-9. PubMed PMID: 18383373.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - A B cell apotope of Ro 60 in systemic lupus erythematosus. AU - Reed,Joanne H, AU - Jackson,Michael W, AU - Gordon,Tom P, PY - 2008/4/3/pubmed PY - 2008/5/22/medline PY - 2008/4/3/entrez SP - 1125 EP - 9 JF - Arthritis and rheumatism JO - Arthritis Rheum. VL - 58 IS - 4 N2 - OBJECTIVE: Previous studies have attempted to segregate anti-60-kd Ro/SSA (anti-Ro 60) responses in systemic lupus erythematosus (SLE) and primary Sjögren's syndrome (SS) but have shown limited disease preference. The aim of the present study was to determine whether the presence of autoantibodies against an Ro 60 apotope (an epitope expressed on apoptotic cells) distinguishes anti-Ro 60 responses in SLE and primary SS. METHODS: Multiparameter flow cytometry was used to select early apoptotic cells and measure the simultaneous binding of annexin V, propidium iodide, and anti-Ro 60-positive IgG from SLE patients (n=21) and patients with primary SS (n=19). The specificity of the Ro 60 apotope was determined by inhibition experiments with recombinant and native Ro 60. RESULTS: Autoantibodies against the Ro 60 apotope were prevalent in SLE patients (13 of 21, 62%) and were rarely observed in patients with primary SS (1 of 19, 5%) (P=0.0002). Further, within SLE patients, autoantibodies to the Ro 60 apotope strongly distinguished patients with anti-Ro 60 alone (12 of 13, 92%) from those with both anti-Ro 60 and anti-La (1 of 8, 13%) (P=0.0005). When we considered all patients with anti-Ro 60 alone, the presence of autoantibodies to the Ro 60 apotope had both high sensitivity (92.3%) and high specificity (85.7%) for SLE compared with primary SS (P=0.0012). The presence of autoantibodies to the Ro 60 apotope may therefore be of diagnostic value in patients with isolated anti-Ro 60 responses. CONCLUSION: The preferential targeting of an Ro 60 apotope exposed on early apoptotic cells in a subset of SLE patients implies disease-specific pathways for the induction of anti-Ro 60 autoimmunity. SN - 0004-3591 UR - https://www.unboundmedicine.com/medline/citation/18383373/A_B_cell_apotope_of_Ro_60_in_systemic_lupus_erythematosus_ L2 - https://doi.org/10.1002/art.23377 DB - PRIME DP - Unbound Medicine ER -