The epitopes recognized by these antibodies were mapped by expression of subfragments of p68 cDNA in Escherichia coli and testing of the corresponding recombinant proteins for immunoreactivity with sera of patients with autoimmune diseases.
The epitopes recognized by these antibodies were mapped by expression of subfragments of p68 cDNA in Escherichia coli and testing of the corresponding recombinant proteins for immunoreactivity with sera of patients with autoimmune diseases.
Previous studies led to the isolation of two overlapping cDNA clones that encode polypeptides of TPO (85 residues, C2; 100 residues, C21) recognized by sera from several patients with autoimmune disease that contained antimicrosomal autoantibodies.
Deregulated IL-6 gene expression has been implicated as being involved in the pathogenesis of a number of diseases, especially autoimmune diseases and plasma cell neoplasias.
Human fibrillarin expressed in vitro migrates on SDS gels as a 36-kDa protein that is specifically immunoprecipitated by antisera from humans with scleroderma autoimmune disease.
Until these mechanisms are understood, clinicians should periodically check their patients with IDDM for other organ-specific as well as non--organ-specific autoimmune diseases.
Abnormal production of IL-6 has been suggested to be involved in glomerulonephritis, plasmacytomagenesis and in the pathogenesis of autoimmune diseases.
In general, the HLA-linked genetic susceptibility to IDDM, as well as to other autoimmune diseases, appears to be associated with specific combinations of class II epitopes (e.g., alleles, haplotypes, or genotypes) rather than with specific individual residues or epitopes.
However, there are still many important questions to be addressed, such as the nature of thymic education, tolerance, the mechanism of MHC-restricted antigen recognition and the relation between TCR repertoire and autoimmunity.
TCR gene usage is also restricted in experimental autoimmune disease, in T cells within organs like skin and other epithelial tissues, and in the brain of patients with multiple sclerosis (MS).
Determination of an epitope of the diffuse systemic sclerosis marker antigen DNA topoisomerase I: sequence similarity with retroviral p30gag protein suggests a possible cause for autoimmunity in systemic sclerosis.
In vivo-activated interleukin 2 receptor-positive T lymphocytes (Tac cells) are demonstrable and the autologous mixed leukocyte reaction (AMLR) is impaired in several autoimmune diseases, including type 1 insulin-dependent diabetes mellitus (IDDM).
Frequent gene deletions and duplications have been described in the C4 and CYP21 genes, particularly in patients with autoimmune diseases and congenital adrenal hyperplasia.
Genetic deficiency of the second component of complement (C2) is the most common complement-deficiency state among Western Europeans and is frequently associated with autoimmune diseases.
Autoimmune diseases or serologic changes are known to have affected relatives of 5 patients, including 4 who had 1 or more relatives with BFP reactions.
The IL-2 receptor is proving to be an extraordinarily versatile therapeutic target, since it is expressed by the abnormal T cells in patients with certain lymphoid malignancies or autoimmune disorders and in individuals rejecting allografts, whereas it is not expressed by normal resting cells.
As discussed in this review, the data so far indicate that a few amino acid substitutions in class II molecules may exert a critical influence on susceptibility to autoimmune diseases such as RA and IDDM.