Avtor/Urednik     Božič, B; Pruijn, GJM; Rozman, B; van Venrooij, WJ
Naslov     Sera from patients with rheumatic diseases recognize different epitope regions on the 52-kD Ro/SS-A protein
Tip     članek
Vir     Clin Exp Immunol
Vol. in št.     Letnik 94, št. 2
Leto izdaje     1993
Obseg     str. 227-35
Jezik     eng
Abstrakt     Patients suffering from systemic lupus erythematosus (SLE) or Sjogren's syndrome (SS) often contain autoantibodies directed to the Ro(SS-A) complex. In this study the antigenic determinants on two of the components of the Ro complex, i.e. the Ro60 and the Ro52 polypeptides, were investigated. Anti-Ro+ sera were selected by counter-immunoelectrophoresis. Depending on the detection method, 59-68 percent of the SLE patients produced anti-Ro but not anti-La antibody, while 72-81 percent of the SS patients produced both anti-Ro and anti-La antibody. Immunoprecipitation of recombinant Ro-proteins showed that 61 sera (87 percent) were reactive with both Ro proteins, seven sera with Ro60 only, one serum with Ro52 only, and one serum did not precipitate the proteins at all. The anti-Ro60 reactivity of human sera is strongly associated with the native form of Ro60, suggesting that conformational autoepitopes are an important feature of Ro60. In the case of Ro52, frequently the residues located between amino acids 216 and 292 were essential for reactivity with the antibodies. With 70 percent of the lupus sera tested this appeared to be the only region important for reactivity. The antibodies of SS patients generally recognized multiple B cell epitopes located between amino acids 55 and 292. The results of this study indicate that the antigenic determinants on Ro52 are different for autoantibodies produced by lupus patients compared with those of SS patients.
Deskriptorji     ANTIBODIES, ANTINUCLEAR
AUTOANTIGENS
RHEUMATIC DISEASES
RIBONUCLEOPROTEINS
ADOLESCENCE
ADULT
AGED
AGED, 80 AND OVER
ANTIBODY SPECIFICITY
ANTIGENIC DETERMINANTS
AUTOANTIGENS
DNA, COMPLEMENTARY
LUPUS ERYTHEMATOSUS, SYSTEMIC
MIDDLE AGE
MUTAGENESIS
RIBONUCLEOPROTEINS
SEQUENCE DELETION
SJOGREN'S SYNDROME