Abstract
Until 4 years ago, PBC could only be classified as an autoimmune liver disease characterized by biliary obstruction and the presence of high titer of AMA. Using the tools of molecular biology, the molecular structures of the autoantigens as well as the B-cell epitopes have been defined within a relatively short time. However, the mechanism of how these subcellular enzymes become autoantigens is still unclear. Is the antibody response antigen driven or the result of molecular mimicry? With the rapid accumulation of information as well as unique reagents such as cDNA clones, recombinant proteins, monoclonal antibodies, it is possible to address questions on the possible mechanisms by which these mitochondrial proteins can become the target of immune response and how these responses are related to the pathogenesis of PBC. The attainment of these challenging goals and directions will be of substantial value in understanding the role of subcellular molecular interactions in the development of autoimmunity.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 518-527 |
| Number of pages | 10 |
| Journal | Immunologic Research |
| Volume | 10 |
| Issue number | 3-4 |
| DOIs | |
| State | Published - Dec 1991 |
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ASJC Scopus subject areas
- Immunology
Cite this
Molecular characterization of the mitochondrial autoantigens in primary biliary cirrhosis. / Leung, Patrick S; Van de Water, Judith A; Coppel, Ross L.; Gershwin, M. Eric.
In: Immunologic Research, Vol. 10, No. 3-4, 12.1991, p. 518-527.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Molecular characterization of the mitochondrial autoantigens in primary biliary cirrhosis
AU - Leung, Patrick S
AU - Van de Water, Judith A
AU - Coppel, Ross L.
AU - Gershwin, M. Eric
PY - 1991/12
Y1 - 1991/12
N2 - Until 4 years ago, PBC could only be classified as an autoimmune liver disease characterized by biliary obstruction and the presence of high titer of AMA. Using the tools of molecular biology, the molecular structures of the autoantigens as well as the B-cell epitopes have been defined within a relatively short time. However, the mechanism of how these subcellular enzymes become autoantigens is still unclear. Is the antibody response antigen driven or the result of molecular mimicry? With the rapid accumulation of information as well as unique reagents such as cDNA clones, recombinant proteins, monoclonal antibodies, it is possible to address questions on the possible mechanisms by which these mitochondrial proteins can become the target of immune response and how these responses are related to the pathogenesis of PBC. The attainment of these challenging goals and directions will be of substantial value in understanding the role of subcellular molecular interactions in the development of autoimmunity.
AB - Until 4 years ago, PBC could only be classified as an autoimmune liver disease characterized by biliary obstruction and the presence of high titer of AMA. Using the tools of molecular biology, the molecular structures of the autoantigens as well as the B-cell epitopes have been defined within a relatively short time. However, the mechanism of how these subcellular enzymes become autoantigens is still unclear. Is the antibody response antigen driven or the result of molecular mimicry? With the rapid accumulation of information as well as unique reagents such as cDNA clones, recombinant proteins, monoclonal antibodies, it is possible to address questions on the possible mechanisms by which these mitochondrial proteins can become the target of immune response and how these responses are related to the pathogenesis of PBC. The attainment of these challenging goals and directions will be of substantial value in understanding the role of subcellular molecular interactions in the development of autoimmunity.
UR - http://www.scopus.com/inward/record.url?scp=0025830984&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0025830984&partnerID=8YFLogxK
U2 - 10.1007/BF02919751
DO - 10.1007/BF02919751
M3 - Article
C2 - 1720161
AN - SCOPUS:0025830984
VL - 10
SP - 518
EP - 527
JO - Immunologic Research
JF - Immunologic Research
SN - 0257-277X
IS - 3-4
ER -