This competitor from a lupus spleen chromatographed on phosphocellulose and showed size fractionation during gel filtration similar to known p27 to p30 viral proteins.
This competitor from a lupus spleen chromatographed on phosphocellulose and showed size fractionation during gel filtration similar to known p27 to p30 viral proteins.
This competitor from a lupus spleen chromatographed on phosphocellulose and showed size fractionation during gel filtration similar to known p27 to p30 viral proteins.
This competitor from a lupus spleen chromatographed on phosphocellulose and showed size fractionation during gel filtration similar to known p27 to p30 viral proteins.
This competitor from a lupus spleen chromatographed on phosphocellulose and showed size fractionation during gel filtration similar to known p27 to p30 viral proteins.
This competitor from a lupus spleen chromatographed on phosphocellulose and showed size fractionation during gel filtration similar to known p27 to p30 viral proteins.
This competitor from a lupus spleen chromatographed on phosphocellulose and showed size fractionation during gel filtration similar to known p27 to p30 viral proteins.
This competitor from a lupus spleen chromatographed on phosphocellulose and showed size fractionation during gel filtration similar to known p27 to p30 viral proteins.
This competitor from a lupus spleen chromatographed on phosphocellulose and showed size fractionation during gel filtration similar to known p27 to p30 viral proteins.
Three families having more than one affected member with SLE or lupus-like disease were investigated by global coagulation tests as well as methods based on dilute thromboplastin, Russell's viper venom and thermal stability/absorption, and by RIA for anticardiolipin (CL) antibodies.
These data demonstrate that anti-Ro(SS-A)/La(SS-B) positive Sjogren's/lupus overlap patients and neonatal lupus syndrome mothers are immunogenetically closely related to each other and appear to be more closely related to both primary Sjogren's syndrome and subacute lupus erythematosus, than to classical systemic lupus erythematosus.
A rabbit antiserum raised against an NH2-terminal peptide, a well-characterized murine monoclonal antibody (mAb), and 14 human lupus sera with autoantibody to PCNA were analyzed for their reactivity with the constructs using both immunoprecipitation and immunoblotting techniques.
Neonatal lupus erythematosus (NLE) is a distinct subset of lupus characterized by cutaneous findings (50%), cardiac conduction defects (50%), and autoantibodies to Ro (SS-A) antigen.
We have analyzed the roles of tumor necrosis factor alpha (TNF-alpha) in human systemic lupus erythematosus (SLE) and murine models of lupus as well as in type 1 diabetes in NOD mice.
Neonatal lupus erythematosus (NLE) is a distinct subset of lupus characterized by cutaneous findings (50%), cardiac conduction defects (50%), and autoantibodies to Ro (SS-A) antigen.
The two infants with CCHB examined were C4B protein-deficient, in contrast to infants with lupus dermatitis, who had frequent C4B null allotypes but no C4B protein deficiency.
HLA typing is reported on these infants, their mothers, and two additional infant-mother pairs with U1RNP antibody-positive lupus whose clinical features have been reported previously.
We have analyzed the roles of tumor necrosis factor alpha (TNF-alpha) in human systemic lupus erythematosus (SLE) and murine models of lupus as well as in type 1 diabetes in NOD mice.
Characterization of type I complement C2 deficiency MHC haplotypes. Strong conservation of the complotype/HLA-B-region and absence of disease association due to linked class II genes.
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.
While patients with anti-RNP precipitin showed an increased frequency of the DQw8-associated allele DQB1*0302 (P = 0.02, OR = 3.7) compared with normal controls, as well as an increased frequency of the DQw5-associated alleles DQA1*0101 and DQB1*0501 (P = 0.05, OR = 4.2) compared with lupus patients without anti-Sm or RNP.