Immunohistochemical Characterization of Hepatic Lymphocytes in Primary Biliary Cirrhosis in Comparison With Primary Sclerosing Cholangitis and Autoimmune Chronic Active Hepatitis
We analyzed the immunophenotypes of hepatic cellular infiltrates by quantitative immunohistochemical methods in biopsy specimens from 20 patients with primary biliary cirrhosis (PBC), 19 with primary sclerosing cholangitis, and 11 with autoimmune chronic active hepatitis. Specifically, we sought to...
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| Veröffentlicht in: | Mayo Clinic proceedings 1993-11, Vol.68 (11), p.1049-1055 |
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| creator | HASHIMOTO, ETSUKO LINDOR, KEITH D. HOMBURGER, HENRY A. DICKSON, E. ROLLAND CZAJA, ALBERT J. WIESNER, RUSSELL H. LUDWIG, JURGEN |
| description | We analyzed the immunophenotypes of hepatic cellular infiltrates by quantitative immunohistochemical methods in biopsy specimens from 20 patients with primary biliary cirrhosis (PBC), 19 with primary sclerosing cholangitis, and 11 with autoimmune chronic active hepatitis. Specifically, we sought to identify activated T cells, interferon-γ-producing cells, and natural killer cells. The portal cellular infiltrate in PBC contained a preponderance of CD4 cells in comparison with CD8 cells, with a CD4/CD8 ratio of 2.45:1. The cellular infiltrate in areas of piecemeal necrosis contained mostly CD8 cells. Infiltrating CD8 cells in PBC had the surface phenotype of cytotoxic (CD8-positive, CD11b-negative) cells. Approximately 4% of T cells expressed interleukin 2 receptors. Interferon-γ-staining cells were rarely identified (in less than 2%). cells that expressed the natural killer cell markers CD16, CD56, or CD57 were infrequent, constituting approximately 5% of the cellular infiltrate. The composition of the infiltrates was similar in patients with PBC and chronic active hepatitis. Natural killer cells were twice as common in patients with primary sclerosing cholangitis (P |
| doi_str_mv | 10.1016/S0025-6196(12)60897-0 |
| format | Article |
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ROLLAND ; CZAJA, ALBERT J. ; WIESNER, RUSSELL H. ; LUDWIG, JURGEN</creator><creatorcontrib>HASHIMOTO, ETSUKO ; LINDOR, KEITH D. ; HOMBURGER, HENRY A. ; DICKSON, E. ROLLAND ; CZAJA, ALBERT J. ; WIESNER, RUSSELL H. ; LUDWIG, JURGEN</creatorcontrib><description>We analyzed the immunophenotypes of hepatic cellular infiltrates by quantitative immunohistochemical methods in biopsy specimens from 20 patients with primary biliary cirrhosis (PBC), 19 with primary sclerosing cholangitis, and 11 with autoimmune chronic active hepatitis. Specifically, we sought to identify activated T cells, interferon-γ-producing cells, and natural killer cells. The portal cellular infiltrate in PBC contained a preponderance of CD4 cells in comparison with CD8 cells, with a CD4/CD8 ratio of 2.45:1. The cellular infiltrate in areas of piecemeal necrosis contained mostly CD8 cells. Infiltrating CD8 cells in PBC had the surface phenotype of cytotoxic (CD8-positive, CD11b-negative) cells. Approximately 4% of T cells expressed interleukin 2 receptors. Interferon-γ-staining cells were rarely identified (in less than 2%). cells that expressed the natural killer cell markers CD16, CD56, or CD57 were infrequent, constituting approximately 5% of the cellular infiltrate. The composition of the infiltrates was similar in patients with PBC and chronic active hepatitis. Natural killer cells were twice as common in patients with primary sclerosing cholangitis (P<0.05) as in those with PBC. The inflammatory infiltrates in areas of piecemeal necrosis were similar in the three diseases and differed from those found within the portal area, in that CD8 cells were preponderant. In all three liver diseases, almost 90% of bile ducts expressed class II HLA antigens. These findings support the hypothesis that cytotoxic T cells of either the CD4 or CD8 immunophenotype but not natural killer cells may be involved in the pathogenesis of PBC and chronic active hepatitis. We were unable to identify interferon-γ-producing cells in the inflammatory infiltrates; thus, we cannot conclude that this mechanism is responsible for aberrant expression of class II HLA antigens on bile duct cells.</description><identifier>ISSN: 0025-6196</identifier><identifier>EISSN: 1942-5546</identifier><identifier>DOI: 10.1016/S0025-6196(12)60897-0</identifier><identifier>PMID: 8231268</identifier><identifier>CODEN: MACPAJ</identifier><language>eng</language><publisher>Rochester, MN: Elsevier Inc</publisher><subject>Adult ; Autoimmune Diseases - immunology ; Autoimmune Diseases - metabolism ; Bile Ducts - immunology ; Bile Ducts - metabolism ; Biological and medical sciences ; Cholangitis, Sclerosing - immunology ; Cholangitis, Sclerosing - metabolism ; Gastroenterology. Liver. Pancreas. Abdomen ; Hepatitis, Chronic - immunology ; Hepatitis, Chronic - metabolism ; Humans ; Immunohistochemistry ; Interferon-gamma - biosynthesis ; Killer Cells, Natural - metabolism ; Liver - immunology ; Liver - metabolism ; Liver Cirrhosis, Biliary - immunology ; Liver Cirrhosis, Biliary - metabolism ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Lymphocytes - metabolism ; Medical sciences ; Middle Aged ; Other diseases. Semiology ; T-Lymphocytes - metabolism</subject><ispartof>Mayo Clinic proceedings, 1993-11, Vol.68 (11), p.1049-1055</ispartof><rights>1993 Mayo Foundation for Medical Education and Research</rights><rights>1994 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c389t-698cb3ac426b6a72ba1039e55c2d8fa8c33e80b747f4f67a85574a10a6b2ad973</citedby><cites>FETCH-LOGICAL-c389t-698cb3ac426b6a72ba1039e55c2d8fa8c33e80b747f4f67a85574a10a6b2ad973</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3823697$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8231268$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HASHIMOTO, ETSUKO</creatorcontrib><creatorcontrib>LINDOR, KEITH D.</creatorcontrib><creatorcontrib>HOMBURGER, HENRY A.</creatorcontrib><creatorcontrib>DICKSON, E. ROLLAND</creatorcontrib><creatorcontrib>CZAJA, ALBERT J.</creatorcontrib><creatorcontrib>WIESNER, RUSSELL H.</creatorcontrib><creatorcontrib>LUDWIG, JURGEN</creatorcontrib><title>Immunohistochemical Characterization of Hepatic Lymphocytes in Primary Biliary Cirrhosis in Comparison With Primary Sclerosing Cholangitis and Autoimmune Chronic Active Hepatitis</title><title>Mayo Clinic proceedings</title><addtitle>Mayo Clin Proc</addtitle><description>We analyzed the immunophenotypes of hepatic cellular infiltrates by quantitative immunohistochemical methods in biopsy specimens from 20 patients with primary biliary cirrhosis (PBC), 19 with primary sclerosing cholangitis, and 11 with autoimmune chronic active hepatitis. Specifically, we sought to identify activated T cells, interferon-γ-producing cells, and natural killer cells. The portal cellular infiltrate in PBC contained a preponderance of CD4 cells in comparison with CD8 cells, with a CD4/CD8 ratio of 2.45:1. The cellular infiltrate in areas of piecemeal necrosis contained mostly CD8 cells. Infiltrating CD8 cells in PBC had the surface phenotype of cytotoxic (CD8-positive, CD11b-negative) cells. Approximately 4% of T cells expressed interleukin 2 receptors. Interferon-γ-staining cells were rarely identified (in less than 2%). cells that expressed the natural killer cell markers CD16, CD56, or CD57 were infrequent, constituting approximately 5% of the cellular infiltrate. The composition of the infiltrates was similar in patients with PBC and chronic active hepatitis. Natural killer cells were twice as common in patients with primary sclerosing cholangitis (P<0.05) as in those with PBC. The inflammatory infiltrates in areas of piecemeal necrosis were similar in the three diseases and differed from those found within the portal area, in that CD8 cells were preponderant. In all three liver diseases, almost 90% of bile ducts expressed class II HLA antigens. These findings support the hypothesis that cytotoxic T cells of either the CD4 or CD8 immunophenotype but not natural killer cells may be involved in the pathogenesis of PBC and chronic active hepatitis. We were unable to identify interferon-γ-producing cells in the inflammatory infiltrates; thus, we cannot conclude that this mechanism is responsible for aberrant expression of class II HLA antigens on bile duct cells.</description><subject>Adult</subject><subject>Autoimmune Diseases - immunology</subject><subject>Autoimmune Diseases - metabolism</subject><subject>Bile Ducts - immunology</subject><subject>Bile Ducts - metabolism</subject><subject>Biological and medical sciences</subject><subject>Cholangitis, Sclerosing - immunology</subject><subject>Cholangitis, Sclerosing - metabolism</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Hepatitis, Chronic - immunology</subject><subject>Hepatitis, Chronic - metabolism</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Interferon-gamma - biosynthesis</subject><subject>Killer Cells, Natural - metabolism</subject><subject>Liver - immunology</subject><subject>Liver - metabolism</subject><subject>Liver Cirrhosis, Biliary - immunology</subject><subject>Liver Cirrhosis, Biliary - metabolism</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Lymphocytes - metabolism</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Other diseases. Semiology</subject><subject>T-Lymphocytes - metabolism</subject><issn>0025-6196</issn><issn>1942-5546</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkd2K1EAQhRtR1nH1ERZyIaIX0f5JOsmVzAb3BwYUVvGy6XQqm5IkHbs7C-Nj-YT2zIS59aoazldVp_oQcsXoR0aZ_PRAKc9TySr5nvEPkpZVkdJnZMOqjKd5nsnnZHNGXpJX3v-ilBZVlV2Qi5ILxmW5IX_vx3GZbI8-WNPDiEYPSd1rp00Ah390QDsltkvuYI5vk-z249xbsw_gE5ySbw5H7fbJNQ54qDU611uPR7G246wd-jjhJ4b-DD-YAVyEpse4yg56esQQO_TUJtslWDxYgig5O8WNWxPwCVYDkXtNXnR68PBmrZfkx82X7_Vduvt6e19vd6kRZRVSWZWmEdpkXDZSF7zRjIoK8tzwtux0aYSAkjZFVnRZJwtd5nmRRUbLhuu2KsQleXeaOzv7ewEf1IjewBD9gl28KiSVNGMigvkJNPEo76BT8-lQxag6ZKWOWalDEIpxdcxK0dh3tS5YmhHac9caTtTfrrr2MZbO6cmgP2MicvLo8_MJg_gZTwhOeYMwGWjRgQmqtfgfI_8Adhy1Vg</recordid><startdate>19931101</startdate><enddate>19931101</enddate><creator>HASHIMOTO, ETSUKO</creator><creator>LINDOR, KEITH D.</creator><creator>HOMBURGER, HENRY A.</creator><creator>DICKSON, E. ROLLAND</creator><creator>CZAJA, ALBERT J.</creator><creator>WIESNER, RUSSELL H.</creator><creator>LUDWIG, JURGEN</creator><general>Elsevier Inc</general><general>Mayo Medical Ventures</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19931101</creationdate><title>Immunohistochemical Characterization of Hepatic Lymphocytes in Primary Biliary Cirrhosis in Comparison With Primary Sclerosing Cholangitis and Autoimmune Chronic Active Hepatitis</title><author>HASHIMOTO, ETSUKO ; LINDOR, KEITH D. ; HOMBURGER, HENRY A. ; DICKSON, E. ROLLAND ; CZAJA, ALBERT J. ; WIESNER, RUSSELL H. ; LUDWIG, JURGEN</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c389t-698cb3ac426b6a72ba1039e55c2d8fa8c33e80b747f4f67a85574a10a6b2ad973</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Adult</topic><topic>Autoimmune Diseases - immunology</topic><topic>Autoimmune Diseases - metabolism</topic><topic>Bile Ducts - immunology</topic><topic>Bile Ducts - metabolism</topic><topic>Biological and medical sciences</topic><topic>Cholangitis, Sclerosing - immunology</topic><topic>Cholangitis, Sclerosing - metabolism</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Hepatitis, Chronic - immunology</topic><topic>Hepatitis, Chronic - metabolism</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Interferon-gamma - biosynthesis</topic><topic>Killer Cells, Natural - metabolism</topic><topic>Liver - immunology</topic><topic>Liver - metabolism</topic><topic>Liver Cirrhosis, Biliary - immunology</topic><topic>Liver Cirrhosis, Biliary - metabolism</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Lymphocytes - metabolism</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Other diseases. Semiology</topic><topic>T-Lymphocytes - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HASHIMOTO, ETSUKO</creatorcontrib><creatorcontrib>LINDOR, KEITH D.</creatorcontrib><creatorcontrib>HOMBURGER, HENRY A.</creatorcontrib><creatorcontrib>DICKSON, E. ROLLAND</creatorcontrib><creatorcontrib>CZAJA, ALBERT J.</creatorcontrib><creatorcontrib>WIESNER, RUSSELL H.</creatorcontrib><creatorcontrib>LUDWIG, JURGEN</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Mayo Clinic proceedings</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HASHIMOTO, ETSUKO</au><au>LINDOR, KEITH D.</au><au>HOMBURGER, HENRY A.</au><au>DICKSON, E. ROLLAND</au><au>CZAJA, ALBERT J.</au><au>WIESNER, RUSSELL H.</au><au>LUDWIG, JURGEN</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Immunohistochemical Characterization of Hepatic Lymphocytes in Primary Biliary Cirrhosis in Comparison With Primary Sclerosing Cholangitis and Autoimmune Chronic Active Hepatitis</atitle><jtitle>Mayo Clinic proceedings</jtitle><addtitle>Mayo Clin Proc</addtitle><date>1993-11-01</date><risdate>1993</risdate><volume>68</volume><issue>11</issue><spage>1049</spage><epage>1055</epage><pages>1049-1055</pages><issn>0025-6196</issn><eissn>1942-5546</eissn><coden>MACPAJ</coden><abstract>We analyzed the immunophenotypes of hepatic cellular infiltrates by quantitative immunohistochemical methods in biopsy specimens from 20 patients with primary biliary cirrhosis (PBC), 19 with primary sclerosing cholangitis, and 11 with autoimmune chronic active hepatitis. Specifically, we sought to identify activated T cells, interferon-γ-producing cells, and natural killer cells. The portal cellular infiltrate in PBC contained a preponderance of CD4 cells in comparison with CD8 cells, with a CD4/CD8 ratio of 2.45:1. The cellular infiltrate in areas of piecemeal necrosis contained mostly CD8 cells. Infiltrating CD8 cells in PBC had the surface phenotype of cytotoxic (CD8-positive, CD11b-negative) cells. Approximately 4% of T cells expressed interleukin 2 receptors. Interferon-γ-staining cells were rarely identified (in less than 2%). cells that expressed the natural killer cell markers CD16, CD56, or CD57 were infrequent, constituting approximately 5% of the cellular infiltrate. The composition of the infiltrates was similar in patients with PBC and chronic active hepatitis. Natural killer cells were twice as common in patients with primary sclerosing cholangitis (P<0.05) as in those with PBC. The inflammatory infiltrates in areas of piecemeal necrosis were similar in the three diseases and differed from those found within the portal area, in that CD8 cells were preponderant. In all three liver diseases, almost 90% of bile ducts expressed class II HLA antigens. These findings support the hypothesis that cytotoxic T cells of either the CD4 or CD8 immunophenotype but not natural killer cells may be involved in the pathogenesis of PBC and chronic active hepatitis. We were unable to identify interferon-γ-producing cells in the inflammatory infiltrates; thus, we cannot conclude that this mechanism is responsible for aberrant expression of class II HLA antigens on bile duct cells.</abstract><cop>Rochester, MN</cop><pub>Elsevier Inc</pub><pmid>8231268</pmid><doi>10.1016/S0025-6196(12)60897-0</doi><tpages>7</tpages></addata></record> |
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| ispartof | Mayo Clinic proceedings, 1993-11, Vol.68 (11), p.1049-1055 |
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| subjects | Adult Autoimmune Diseases - immunology Autoimmune Diseases - metabolism Bile Ducts - immunology Bile Ducts - metabolism Biological and medical sciences Cholangitis, Sclerosing - immunology Cholangitis, Sclerosing - metabolism Gastroenterology. Liver. Pancreas. Abdomen Hepatitis, Chronic - immunology Hepatitis, Chronic - metabolism Humans Immunohistochemistry Interferon-gamma - biosynthesis Killer Cells, Natural - metabolism Liver - immunology Liver - metabolism Liver Cirrhosis, Biliary - immunology Liver Cirrhosis, Biliary - metabolism Liver. Biliary tract. Portal circulation. Exocrine pancreas Lymphocytes - metabolism Medical sciences Middle Aged Other diseases. Semiology T-Lymphocytes - metabolism |
| title | Immunohistochemical Characterization of Hepatic Lymphocytes in Primary Biliary Cirrhosis in Comparison With Primary Sclerosing Cholangitis and Autoimmune Chronic Active Hepatitis |
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