DOI Page / Citation link:
https://doi.org/10.11588/diglit.48120#0079
Abstracts
61
autoreactive determinants was performed with a collection of human autoim-
mune sera. Using a large series of fusion proteins in immunoblotting as well as
peptide based ELISAs we identified several independent epitopes a few amino
acids in length and larger sequences which presumably represent discontinuous
epitopes. One of these epitopes is recognized by virtually all anti-p68 antibody
positive sera, another one by appr. 30% and some reacted with less than 10% of
the sera. Patient specific epitope recognition patterns were identified. These data
demonstrate polyclonality of the anti-68 kDa autoimmune response, rule out
somatic mutation as a sole mechanism of anti-68 kDa autoantibody induction,
and argue for an antigen-driven autoimmune response but do not exclude the in-
volvement of microorganisms as autoimmune process initiators by molecular
mimicry. The identification of several independent autoreactive epitopes allows
differential screening for patient specific epitope patterns which may become a
useful tool for diagnosis, prognosis and therapy control.
References
1. Netter, H. J., Guldner, H.H., Szostecki, C., Lakomek, H. J., Will, H. (1988): A
recombinant autoantigen derived from the human (Ul) small nuclear RNP-specific
68-kd protein. Expression in Escherichia coli and serodiagnostic application. Arthritis
Rheum. 31, 616-621
2. Guldner, H.H., Netter, H.J., Szostecki, C., Lakomek, H.J., Will, H. (1988):
Epitope mapping with a recombinant human 68-kDa (U 1) ribonucleoprotein antigen
reveals heterogeneous autoantibody profiles in human autoimmune sera. J. Immunol.
141, 469-475
Current Ideas on Tolerance Mechanisms and Autoimmunity
G.J.V. Nossal
The Walter and Eliza Hall Institute of Medical Research, P. O. Royal Melbourne Hospital,
Victoria 3050, Australia
The work of the last two years has seen some giant strides taken in our
understanding of mechanisms of immunological tolerance. Extensive use of
transgenic animals has provided new models of great power and elegance, though
each model must be carefully analyzed for those features that might introduce
61
autoreactive determinants was performed with a collection of human autoim-
mune sera. Using a large series of fusion proteins in immunoblotting as well as
peptide based ELISAs we identified several independent epitopes a few amino
acids in length and larger sequences which presumably represent discontinuous
epitopes. One of these epitopes is recognized by virtually all anti-p68 antibody
positive sera, another one by appr. 30% and some reacted with less than 10% of
the sera. Patient specific epitope recognition patterns were identified. These data
demonstrate polyclonality of the anti-68 kDa autoimmune response, rule out
somatic mutation as a sole mechanism of anti-68 kDa autoantibody induction,
and argue for an antigen-driven autoimmune response but do not exclude the in-
volvement of microorganisms as autoimmune process initiators by molecular
mimicry. The identification of several independent autoreactive epitopes allows
differential screening for patient specific epitope patterns which may become a
useful tool for diagnosis, prognosis and therapy control.
References
1. Netter, H. J., Guldner, H.H., Szostecki, C., Lakomek, H. J., Will, H. (1988): A
recombinant autoantigen derived from the human (Ul) small nuclear RNP-specific
68-kd protein. Expression in Escherichia coli and serodiagnostic application. Arthritis
Rheum. 31, 616-621
2. Guldner, H.H., Netter, H.J., Szostecki, C., Lakomek, H.J., Will, H. (1988):
Epitope mapping with a recombinant human 68-kDa (U 1) ribonucleoprotein antigen
reveals heterogeneous autoantibody profiles in human autoimmune sera. J. Immunol.
141, 469-475
Current Ideas on Tolerance Mechanisms and Autoimmunity
G.J.V. Nossal
The Walter and Eliza Hall Institute of Medical Research, P. O. Royal Melbourne Hospital,
Victoria 3050, Australia
The work of the last two years has seen some giant strides taken in our
understanding of mechanisms of immunological tolerance. Extensive use of
transgenic animals has provided new models of great power and elegance, though
each model must be carefully analyzed for those features that might introduce