Not surprisingly, total and partial deficiencies of certain complement components and C3b receptors are associated with rheumatic diseases, particularly systemic lupus erythematosus.
Recent investigations on the mechanisms of ANA production in the rheumatic diseases suggest that these responses frequently emerge in the setting of nonspecific immunoregulatory disturbances.
Calpastatin is the natural inhibitor of calpains, which are members of the cysteine proteinases recently implicated in joint destruction in rheumatic diseases.
Families were recruited from the Arthritis and Rheumatism Council's National Repository of RA families and HLA-DRB1 alleles were examined in these individuals and their first degree relatives using DNA typing methods.
These findings support the involvement of the HLA linked LMP2 gene in the expression of disease in B27 individuals and represent a novel finding in rheumatic disease.
We generated "signature" oligonucleotides from these CDR3s and probed PCR amplified V kappa products from the synovium and PBLs of the same patient, and from PBLs and spleen of individuals without rheumatic disease.
Since all of these functions are of potential importance in the induction or maintenance or both of autoimmune disease, samples from the Arthritis and Rheumatism Council's repository of multicase rheumatoid arthritis families were typed for a dinucleotide repeat in the NRAMP1 promoter region and four other 2q34 (TNP1) or 2q35 (IL8R, VIL1, DES) marker genes.
Since all of these functions are of potential importance in the induction or maintenance or both of autoimmune disease, samples from the Arthritis and Rheumatism Council's repository of multicase rheumatoid arthritis families were typed for a dinucleotide repeat in the NRAMP1 promoter region and four other 2q34 (TNP1) or 2q35 (IL8R, VIL1, DES) marker genes.
Since all of these functions are of potential importance in the induction or maintenance or both of autoimmune disease, samples from the Arthritis and Rheumatism Council's repository of multicase rheumatoid arthritis families were typed for a dinucleotide repeat in the NRAMP1 promoter region and four other 2q34 (TNP1) or 2q35 (IL8R, VIL1, DES) marker genes.
LMP-1 deletions associated with certain aggressive lymphoid neoplasms are not required for the genesis of lymphoproliferative disorders in patients with rheumatic disease.
In both patients, HLA typing revealed 3 alleles typically associated with rheumatic diseases: HLA-DRB1*0405 and HLA-DQB1*0302 (associated with RA), and HLA-DRB4*01 (associated with mixed connective tissue disease and autoimmune reactions in patients with silicone breast implants.
In both patients, HLA typing revealed 3 alleles typically associated with rheumatic diseases: HLA-DRB1*0405 and HLA-DQB1*0302 (associated with RA), and HLA-DRB4*01 (associated with mixed connective tissue disease and autoimmune reactions in patients with silicone breast implants.
In both patients, HLA typing revealed 3 alleles typically associated with rheumatic diseases: HLA-DRB1*0405 and HLA-DQB1*0302 (associated with RA), and HLA-DRB4*01 (associated with mixed connective tissue disease and autoimmune reactions in patients with silicone breast implants.
HLA class II allele distributions did not differ among 3 anti-Ro/SS-A positive groups with different disease expressions, i.e., patients with systemic lupus erythematosus, patients with primary Sjögren's syndrome, and women with no apparent symptoms of rheumatic disease.
As a result of this unique combination of the libraries and probes, we cloned follistatin-related protein (FRP) as a novel autoantigen in systemic rheumatic diseases.