Both p8 and p14 of CaBP were found at elevated levels in sera of some patients with connective tissue diseases [highly elevated in rheumatoid arthritis (RA), Sjogren's syndrome (SjS), systemic lupus erythematosus (SLE), and progressive systemic sclerosis (PSS), and moderately in polymyositis or dermatomyositis (PM/DM) and mixed connective tissue disease (MCTD)].
Both p8 and p14 of CaBP were found at elevated levels in sera of some patients with connective tissue diseases [highly elevated in rheumatoid arthritis (RA), Sjogren's syndrome (SjS), systemic lupus erythematosus (SLE), and progressive systemic sclerosis (PSS), and moderately in polymyositis or dermatomyositis (PM/DM) and mixed connective tissue disease (MCTD)].
Both p8 and p14 of CaBP were found at elevated levels in sera of some patients with connective tissue diseases [highly elevated in rheumatoid arthritis (RA), Sjogren's syndrome (SjS), systemic lupus erythematosus (SLE), and progressive systemic sclerosis (PSS), and moderately in polymyositis or dermatomyositis (PM/DM) and mixed connective tissue disease (MCTD)].
Both p8 and p14 of CaBP were found at elevated levels in sera of some patients with connective tissue diseases [highly elevated in rheumatoid arthritis (RA), Sjogren's syndrome (SjS), systemic lupus erythematosus (SLE), and progressive systemic sclerosis (PSS), and moderately in polymyositis or dermatomyositis (PM/DM) and mixed connective tissue disease (MCTD)].
Both p8 and p14 of CaBP were found at elevated levels in sera of some patients with connective tissue diseases [highly elevated in rheumatoid arthritis (RA), Sjogren's syndrome (SjS), systemic lupus erythematosus (SLE), and progressive systemic sclerosis (PSS), and moderately in polymyositis or dermatomyositis (PM/DM) and mixed connective tissue disease (MCTD)].
Using molecular genetic tools in serologically homogeneous patient populations, and across racial lines, the Ro (SS-A) and la (SS-B) autoantibody responses in systemic lupus erythematosus and Sjögren's syndrome appear to associate most strongly with HLA-DQ alleles, whereas the anti-Jo-1 autoantibody in myositis correlates best with HLA-DRw52.
Using molecular genetic tools in serologically homogeneous patient populations, and across racial lines, the Ro (SS-A) and la (SS-B) autoantibody responses in systemic lupus erythematosus and Sjögren's syndrome appear to associate most strongly with HLA-DQ alleles, whereas the anti-Jo-1 autoantibody in myositis correlates best with HLA-DRw52.
Because the SS-A/Ro and SS-B/La autoantibody responses in SS and systemic lupus erythematosus (SLE) show even stronger correlations with HLA alleles, HLA-DR and DQ alleles were examined using restriction fragment length polymorphisms (RFLP) in white and black patients with SS and/or SS having anti-Ro and anti-La antibodies.
Because the SS-A/Ro and SS-B/La autoantibody responses in SS and systemic lupus erythematosus (SLE) show even stronger correlations with HLA alleles, HLA-DR and DQ alleles were examined using restriction fragment length polymorphisms (RFLP) in white and black patients with SS and/or SS having anti-Ro and anti-La antibodies.
Because the SS-A/Ro and SS-B/La autoantibody responses in SS and systemic lupus erythematosus (SLE) show even stronger correlations with HLA alleles, HLA-DR and DQ alleles were examined using restriction fragment length polymorphisms (RFLP) in white and black patients with SS and/or SS having anti-Ro and anti-La antibodies.
The frequency of HLA-A, -B, and -DR alloantigens was studied in 46 patients with primary Sjögren's syndrome (pSS), 14 patients with secondary Sjögren's syndrome (sSS) and rheumatoid arthritis (RA), 26 classical RA patients without clinical or histologic evidence of Sjögren's syndrome (SS) and 172 normal controls.
The results of the present study indicate that the 'SS susceptibility gene' in Greek patients is linked with the HLA-DR5 expression gene and they support the hypothesis that the fundamental pSS gene may belong to another locus.
Almost all systems showed a considerable range of gene frequency among the various subgroups of patients with SS but only a few attained statistical significance (C3 and GPT).
We have found the Ro (SS-A) antibody with increased frequency in idiopathic thrombocytopenic purpura and thrombocytopenia associated with Sjögren's syndrome, but the nature of the association is unknown.
We have found the Ro (SS-A) antibody with increased frequency in idiopathic thrombocytopenic purpura and thrombocytopenia associated with Sjögren's syndrome, but the nature of the association is unknown.
Thus, HLA-DR3 and DRw6 Ro(SS-A) positive SS/LE patients may possess a similar, if not unique, DR region DNA nucleotide sequence involved in disease susceptibility or immune regulation.
Other 'auto-immune' phenomena such as Sjogren's-like syndrome and polyarthritis were present in association with antibodies to RNP, low C4 and a null allele was demonstrated at the C4B locus.
Patients with Sjögren's syndrome (SS) in association with either Rheumatoid Arthritis (RA), Systemic Lupus Erythematosus (SLE) or Sclerodactyly were tested for HLA-A, B and Dr antigens and the phenotypes of the 4th component of complement (CA).
Exciting links between genetic phenotypes, certain immune responses, and related cutaneous findings in neonatal, complement-deficient, subacute cutaneous, and ANA-negative lupus erythematosus and Sjögren's syndrome have been found.
Although primary and secondary SS were most strongly associated with this DS specificity (MT2), the anti-Ro (SS-A) and anti-La (SS-B) antibody responses were more closely allied to DR antigens.
Although primary and secondary SS were most strongly associated with this DS specificity (MT2), the anti-Ro (SS-A) and anti-La (SS-B) antibody responses were more closely allied to DR antigens.