Quantitative assessment of antibodies to ribonucleoproteins in primary Sjögren’s syndrome : correlation with B cell biomarkers and disease activity

S Candon ¹, JE Gottenberg ², D Bengoufa ³, L Chatenoud ¹ and X Mariette ^2*

¹ Immunology, Necker Hospital, Paris, France
² Rheumatology, Bicetre hospital, Le Kremlin Bicetre, France
³ Immunology, Saint-Louis Hospital, Paris, France

^* To whom correspondence should be addressed. E-mail: xavier.mariette{at}bct.ap-hop-paris.fr.

Accepted 26 July 2008

Abstract

Objective: Detection of antibodies to ribonucleoproteins represents a major diagnostic tool in primary Sjögren’s syndrome (pSS). We assessed the added value of using a radioligand assay compared to ELISA to detect antibodies to SSA, SSB and RNP and analyzed the correlation between autoantibody levels, B-cell biomarkers and disease activity.

Patients and methods: Antibodies to SSA, SSB and RNP were assessed in 127 patients with pSS using a radioligand assay (RLA) and ELISA. In parallel, parameters of B cell activation were measured including serum levels of BAFF.

Results: The RLA showed a better sensitivity as compared to ELISA for the detection of antibodies to SSB (59% of positive samples versus 37% respectively) and antibodies to RNP (9% versus 3%). No difference was observed for the sensitivity of detection of antibodies to SSA. Anti-SSA and anti-SSB levels were correlated with both techniques. Mean levels of antibodies to SSA were significantly higher in patients presenting both antibodies to SSA and SSB compared to those exhibiting only antibodies to SSA. Levels of antibodies to SSA and SSB significantly correlated with those of circulating BAFF (r=0.4, P= 0.004 and r= 0.6, P= 0.0001, respectively) and with B cell biomarkers, including levels of gammaglobulins, beta2-microglobulin, and rheumatoid factor.

Conclusion: RLA allowed a quantitative and more sensitive detection of antibodies to SSB and RNP in pSS. Quantitative assessment of autoantibodies might reveal a biomarker of disease activity and help to get further insights into the pathogenesis of the spreading of the autoantibody response.