Ro/SSA and La/SSB specific IgA autoantibodies in serum of patients with Sjogren's syndrome and systemic lupus erythematosus

Citation
N. Pourmand et al., Ro/SSA and La/SSB specific IgA autoantibodies in serum of patients with Sjogren's syndrome and systemic lupus erythematosus, ANN RHEUM D, 58(10), 1999, pp. 623-629
Citations number
46
Categorie Soggetti
Rheumatology,"da verificare
Journal title
ANNALS OF THE RHEUMATIC DISEASES
ISSN journal
00034967 → ACNP
Volume
58
Issue
10
Year of publication
1999
Pages
623 - 629
Database
ISI
SICI code
0003-4967(199910)58:10<623:RALSIA>2.0.ZU;2-T
Abstract
Objective-To investigate the occurrence of IgA autoantibodies to Ro 52 kDa, Ro 60 kDa and La antigen in serum of patients with primary Sjogren's syndr ome (pSS) and systemic lupus erythematosus (SLE). Methods-Recombinant Ro 52 kDa, Ro 60 kDa and La antigens were used to analy se autoantibodies in serum from 25 patients with pSS, 30 patients with SLE and 20 controls using a semiquantitative immunoblotting approach. Results-Among the patients with pSS, 21 (84%) had detectable IgA autoantibo dies to Ro 52 kDa, 13 (52%) to Ro 60 kDa and 20 (80%) to La antigen. The co rresponding results for the patients with SLE were 22 (73%), 14 (47%) and 2 0 (67%), respectively. No IgA autoantibodies against the three antigens wer e detected in 20 normal controls. A comparison of several clinical features with the titres of IgA antibodies to Ro 52 kDa, Ro 60 kDa and La, revealed a significant relation between IgA anti-Ro 52 and IgA anti-La to sicca (p < 0.05). Semiquantitative data suggest that IgG is the dominating antibody to the three antigens followed by IgM > IgA in both SLE and pSS patients. S pecificity studies of IgA autoantibodies with different subfragments of Ro 52 kDa and Ro 60 kDa antigens showed that IgA antibodies did not differ fro m IgG and IgM in their recognition pattern. Conclusion-These results suggest that besides IgM and IgG, IgA autoantibodi es are also detected at high frequency in patients with pSS and SLE. Furthe r studies are necessary to evaluate the contribution of these IgA autoantib odies to inflammation as well as their diagnostic value.