Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1991-6-11
pubmed:abstractText
Autoantibodies against microsomal antigen of liver and kidney (LKM-1) are diagnostic markers for a subgroup of autoimmune chronic active hepatitis (AI-CAH). Cytochrome P450dbl, now classified as cytochrome P450 IID6, is the major antigen of LKM-1 antibodies. Immunohistological studies suggest that hepatic injury in AI-CAH is mediated by liver-infiltrating T cells. In the present study the specificity and function of liver-infiltrating T cells was analysed at the clonal level. Phenotypical characterization of 189 T cell clones isolated from four liver biopsies of LKM-1 antibody-positive patients showed an enrichment of CD4+ CD8- T cell clones proliferated specifically in the presence of recombinant human LKM-1 antigen (rLKM). This reaction was restricted to autologous antigen-presenting cells and to HLA class II molecules. In order to see whether rLKM was also recognized by peripheral blood T lymphocytes (PBL) we tested the proliferative response of PBL from several individuals. PBL from three of the four patients with LKM-1 antibody-positive AI-CAH proliferated to rLKM, whereas no response was seen with PBL from patients with LKM-1 antibody-negative chronic liver diseases and from healthy blood donors. These data demonstrate that the LKM-1 antigen is recognized by liver-infiltrating T cells in LKM-1 antibody-positive AI-CAH. For further functional characterization, liver-derived T cell clones were tested for their cytotoxic activity. In the presence of phytohaemagglutinin 24 out of 26 CD4- CD8+ but also 20 out of 63 CD4+ CD8- T cell clones lysed autologous as well as allogenic EBV-transformed B cell lines or K562 cells. Five CD4- CD8+ T cell clones lysed autologous but not allogenic B cell lines spontaneously in a HLA class I-restricted manner. Although the antigen specificity of these clones is still unknown the data show the presence of autoreactive T cells at the site of inflammation that could contribute in the pathogenesis of AI-CAH.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/2025956-2391070, http://linkedlifedata.com/resource/pubmed/commentcorrection/2025956-2420472, http://linkedlifedata.com/resource/pubmed/commentcorrection/2025956-2466049, http://linkedlifedata.com/resource/pubmed/commentcorrection/2025956-2477450, http://linkedlifedata.com/resource/pubmed/commentcorrection/2025956-2503564, http://linkedlifedata.com/resource/pubmed/commentcorrection/2025956-2572541, http://linkedlifedata.com/resource/pubmed/commentcorrection/2025956-2681396, http://linkedlifedata.com/resource/pubmed/commentcorrection/2025956-2957133, http://linkedlifedata.com/resource/pubmed/commentcorrection/2025956-3123997, http://linkedlifedata.com/resource/pubmed/commentcorrection/2025956-3186722, http://linkedlifedata.com/resource/pubmed/commentcorrection/2025956-3308211, http://linkedlifedata.com/resource/pubmed/commentcorrection/2025956-3679093, http://linkedlifedata.com/resource/pubmed/commentcorrection/2025956-4587503, http://linkedlifedata.com/resource/pubmed/commentcorrection/2025956-6187843, http://linkedlifedata.com/resource/pubmed/commentcorrection/2025956-6307807, http://linkedlifedata.com/resource/pubmed/commentcorrection/2025956-6406607, http://linkedlifedata.com/resource/pubmed/commentcorrection/2025956-6467682, http://linkedlifedata.com/resource/pubmed/commentcorrection/2025956-71400
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0009-9104
pubmed:author
pubmed:issnType
Print
pubmed:volume
84
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
297-302
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Clonal analysis of liver-infiltrating T cells in patients with LKM-1 antibody-positive autoimmune chronic active hepatitis.
pubmed:affiliation
First Department of Medicine, University of Mainz, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't