DOI Page / Citation link:
https://doi.org/10.11588/diglit.48120#0069
Abstracts
51
they have kinetochore autoantibodies (3/25) and specifically that the serum an-
tibodies of dSSc patients do not react with this antigen (0/55). In 100 sera from
Red cross volunteers we found one serum positive for these specific dots by immu-
nofluorescence but it was negative with the cloned antigen. The minor overlap
recognized with PBC patients sera corresponds to the kinetochore and may select
patients with an overlap syndrome.
Determination of an Epitope of the Diffuse Scleroderma Marker
Antigen Topoisomerase I. Sequence Similarity with Retroviral p30gag
Protein Suggests a Possible Cause for Autoimmunity in Scleroderma
G. G. Maul, S. A. Juminez, and D. Ziemnicka-Kotula
Wistar Institute of Anatomy and Biology, 36th and Spruce Streets, Philadelphia,
PA 19104, USA
Department of Medicine Thomas Jefferson University, 1020 Locust Street, Philadelphia,
PA 19107, USA
The possibility that viruses play a role in the etiology of various autoimmune
diseases has been proposed. One approach to the search for these agents involves
identifying potential crossreactive epitopes in viruses that infect cells of the im-
mune system or of the target tissues. Anti-topoisomerase I antibodies are the
marker autoantibodies for diffuse systemic sclerosis (dSSc). The major epitope of
the antigen was therefore sought through cloning and sequencing of the cDNA
for human topoisomerase I and eventually by the synthesis of the smallest possi-
ble peptide recognized by sera from patients with the diffuse form of systemic
sclerosis. Of two potential antigenic 11 amino acid sequences one contained 6 se-
quential amino acids that are identical to a sequence present in the group-specific
antigen (p30gag) of some mammalian retroviruses. This sequence was recognized
by many dSSc patients sera. It is separated by only one amino acid from the
retroviral epitope sequence that crossreacts with autoantibodies against the mixed
connective-tissue disease and systemic lupus erythromatosus marker antigen (Ut)
RNP (60 kDa). These findings suggest that a retroviral agent may be involved in
the pathogenesis of scleroderma, and other connective tissue diseases and that an-
tibodies to intracellular autoantigens are not involved in the pathogenesis of
autoimmune disease but may be useful as footprints for tracking the potential
etiological agent of autoimmune disease.
51
they have kinetochore autoantibodies (3/25) and specifically that the serum an-
tibodies of dSSc patients do not react with this antigen (0/55). In 100 sera from
Red cross volunteers we found one serum positive for these specific dots by immu-
nofluorescence but it was negative with the cloned antigen. The minor overlap
recognized with PBC patients sera corresponds to the kinetochore and may select
patients with an overlap syndrome.
Determination of an Epitope of the Diffuse Scleroderma Marker
Antigen Topoisomerase I. Sequence Similarity with Retroviral p30gag
Protein Suggests a Possible Cause for Autoimmunity in Scleroderma
G. G. Maul, S. A. Juminez, and D. Ziemnicka-Kotula
Wistar Institute of Anatomy and Biology, 36th and Spruce Streets, Philadelphia,
PA 19104, USA
Department of Medicine Thomas Jefferson University, 1020 Locust Street, Philadelphia,
PA 19107, USA
The possibility that viruses play a role in the etiology of various autoimmune
diseases has been proposed. One approach to the search for these agents involves
identifying potential crossreactive epitopes in viruses that infect cells of the im-
mune system or of the target tissues. Anti-topoisomerase I antibodies are the
marker autoantibodies for diffuse systemic sclerosis (dSSc). The major epitope of
the antigen was therefore sought through cloning and sequencing of the cDNA
for human topoisomerase I and eventually by the synthesis of the smallest possi-
ble peptide recognized by sera from patients with the diffuse form of systemic
sclerosis. Of two potential antigenic 11 amino acid sequences one contained 6 se-
quential amino acids that are identical to a sequence present in the group-specific
antigen (p30gag) of some mammalian retroviruses. This sequence was recognized
by many dSSc patients sera. It is separated by only one amino acid from the
retroviral epitope sequence that crossreacts with autoantibodies against the mixed
connective-tissue disease and systemic lupus erythromatosus marker antigen (Ut)
RNP (60 kDa). These findings suggest that a retroviral agent may be involved in
the pathogenesis of scleroderma, and other connective tissue diseases and that an-
tibodies to intracellular autoantigens are not involved in the pathogenesis of
autoimmune disease but may be useful as footprints for tracking the potential
etiological agent of autoimmune disease.