@article{9787,
  keywords = {Amino Acid Sequence, Antibodies, Antinuclear, Autoimmune Diseases, Base Sequence, Binding Sites, Antibody, DNA, Humans, Hybridomas, Immunoglobulin Heavy Chains, Immunoglobulin kappa-Chains, Immunoglobulin M, Immunoglobulin Variable Region, leprosy, Molecular Sequence Data},
  author = {Dersimonian H and McAdam K P and Mackworth-Young C and Stollar B D},
  title = {The recurrent expression of variable region segments in human IgM anti-DNA autoantibodies.},
  abstract = {<p>RNA sequences for the V regions of human hybridoma-produced autoantibodies were determined by primer extension with reverse transcriptase. The sequencing of IgM autoantibodies from a leprosy patient revealed examples of recurrent use of V region gene segments in different autoantibodies from this patient and a previously studied patient with SLE. Moreover, several gene segments used in these autoantibodies show little alteration from germ-line sequences. mAb TH3, from a patient with leprosy, binds denatured DNA and poly(dT). The center of its H chain CDR35 has a sequence identical to that found previously in two anti-DNA antibodies from a lupus patient; these identities and their overlapping with two other published sequences define a human D-gene segment of approximately 25 nucleotides. Autoantibody TH9, from a leprosy patient, does not bind DNA. Its VH sequence has 87% identity with a VHI anti-DNA antibody, but differs from it markedly in the CDR1 region. TH9 also has a different H chain CDR3. The closely related JH4 or JH5 gene segments are expressed in five lupus or leprosy autoantibodies. In four of the antibodies, examples of V kappa 1, V kappa 3, or V kappa 4 and J kappa 2, or J kappa 5 segments were found. Two distinct leprosy-derived anti-DNA antibodies, 8E10 and TH3, share a completely identical V kappa sequence. This sequence differs in only two positions from that of a germ-line RF L chain gene. Several gene segments that are close to the germ line in sequence encode Ig V regions with autoantibody reactivity. These results provide a base line for determining whether these genes are precursors of more highly diversified antibodies that may be pathogenic in patients with SLE.</p>},
  year = {1989},
  journal = {Journal of immunology (Baltimore, Md. : 1950)},
  volume = {142},
  pages = {4027-33},
  month = {1989 Jun 01},
  issn = {0022-1767},
  language = {eng},
}