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Deficient interleukin‐2 responsiveness of T lymphocytes from patients with primary biliary cirrhosis
There is increasing evidence that primary biliary cirrhosis is associated with an alteration of the immune system. Although the cause remains unknown, it has been suggested that the immune system of patients with primary biliary cirrhosis is involved in the pathogenesis of their disease. We have inv...
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Published in: | Hepatology (Baltimore, Md.) Md.), 1992-10, Vol.16 (4), p.931-936 |
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container_title | Hepatology (Baltimore, Md.) |
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creator | Menéndez, José Luis Girón, José Antonio Manzano, Luis Garrido, Aurelio Abreu, Luis Albillos, Agustin Durántez, Alberto Alvarez‐Mon, Melchor |
description | There is increasing evidence that primary biliary cirrhosis is associated with an alteration of the immune system. Although the cause remains unknown, it has been suggested that the immune system of patients with primary biliary cirrhosis is involved in the pathogenesis of their disease. We have investigated the T‐cell function in patients with primary biliary cirrhosis and have found defective phytohemagglutinin‐induced T‐cell mitogenesis. Likewise, their blastogenic response to CD3 monoclonal antibody was also depressed, although the DNA synthesis induced by stimulation with phorbol esters (12‐O‐tetradecanoilphorbol‐13‐acetate) plus ionophore (ionomycin) was normal. These alterations could not be ascribed either to a decreased synthesis of interleukin‐2 or to a defective expression of interleukin‐2 receptor after cellular activation. Moreover, this defective proliferative response of T lymphocytes was observed even in the presence of saturating concentrations of exogenous interleukin‐2. These results represent evidence of the deficiency in the interleukin‐2—dependent pathway found in T lymphocytes from patients with primary biliary cirrhosis. (HEPATOLOGY 1992;16:931–936.) |
doi_str_mv | 10.1002/hep.1840160413 |
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Although the cause remains unknown, it has been suggested that the immune system of patients with primary biliary cirrhosis is involved in the pathogenesis of their disease. We have investigated the T‐cell function in patients with primary biliary cirrhosis and have found defective phytohemagglutinin‐induced T‐cell mitogenesis. Likewise, their blastogenic response to CD3 monoclonal antibody was also depressed, although the DNA synthesis induced by stimulation with phorbol esters (12‐O‐tetradecanoilphorbol‐13‐acetate) plus ionophore (ionomycin) was normal. These alterations could not be ascribed either to a decreased synthesis of interleukin‐2 or to a defective expression of interleukin‐2 receptor after cellular activation. Moreover, this defective proliferative response of T lymphocytes was observed even in the presence of saturating concentrations of exogenous interleukin‐2. These results represent evidence of the deficiency in the interleukin‐2—dependent pathway found in T lymphocytes from patients with primary biliary cirrhosis. (HEPATOLOGY 1992;16:931–936.)</description><identifier>ISSN: 0270-9139</identifier><identifier>EISSN: 1527-3350</identifier><identifier>DOI: 10.1002/hep.1840160413</identifier><identifier>PMID: 1398499</identifier><identifier>CODEN: HPTLD9</identifier><language>eng</language><publisher>Philadelphia, PA: W.B. Saunders</publisher><subject>Biological and medical sciences ; Cell Division - drug effects ; Gastroenterology. Liver. Pancreas. Abdomen ; Humans ; Interleukin-2 - biosynthesis ; Interleukin-2 - pharmacology ; Liver Cirrhosis, Biliary - pathology ; Liver Cirrhosis, Biliary - physiopathology ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Lymphocyte Activation ; Medical sciences ; Middle Aged ; Other diseases. Semiology ; Phytohemagglutinins - pharmacology ; T-Lymphocytes - drug effects ; T-Lymphocytes - metabolism ; T-Lymphocytes - physiology</subject><ispartof>Hepatology (Baltimore, Md.), 1992-10, Vol.16 (4), p.931-936</ispartof><rights>Copyright © 1992 American Association for the Study of Liver Diseases</rights><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3243-5591c16ea367fefb2956ae87c7322c97c26cf8a97bdf0de31036af5c113284c63</citedby><cites>FETCH-LOGICAL-c3243-5591c16ea367fefb2956ae87c7322c97c26cf8a97bdf0de31036af5c113284c63</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=4443728$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1398499$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Menéndez, José Luis</creatorcontrib><creatorcontrib>Girón, José Antonio</creatorcontrib><creatorcontrib>Manzano, Luis</creatorcontrib><creatorcontrib>Garrido, Aurelio</creatorcontrib><creatorcontrib>Abreu, Luis</creatorcontrib><creatorcontrib>Albillos, Agustin</creatorcontrib><creatorcontrib>Durántez, Alberto</creatorcontrib><creatorcontrib>Alvarez‐Mon, Melchor</creatorcontrib><title>Deficient interleukin‐2 responsiveness of T lymphocytes from patients with primary biliary cirrhosis</title><title>Hepatology (Baltimore, Md.)</title><addtitle>Hepatology</addtitle><description>There is increasing evidence that primary biliary cirrhosis is associated with an alteration of the immune system. Although the cause remains unknown, it has been suggested that the immune system of patients with primary biliary cirrhosis is involved in the pathogenesis of their disease. We have investigated the T‐cell function in patients with primary biliary cirrhosis and have found defective phytohemagglutinin‐induced T‐cell mitogenesis. Likewise, their blastogenic response to CD3 monoclonal antibody was also depressed, although the DNA synthesis induced by stimulation with phorbol esters (12‐O‐tetradecanoilphorbol‐13‐acetate) plus ionophore (ionomycin) was normal. These alterations could not be ascribed either to a decreased synthesis of interleukin‐2 or to a defective expression of interleukin‐2 receptor after cellular activation. Moreover, this defective proliferative response of T lymphocytes was observed even in the presence of saturating concentrations of exogenous interleukin‐2. These results represent evidence of the deficiency in the interleukin‐2—dependent pathway found in T lymphocytes from patients with primary biliary cirrhosis. (HEPATOLOGY 1992;16:931–936.)</description><subject>Biological and medical sciences</subject><subject>Cell Division - drug effects</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Humans</subject><subject>Interleukin-2 - biosynthesis</subject><subject>Interleukin-2 - pharmacology</subject><subject>Liver Cirrhosis, Biliary - pathology</subject><subject>Liver Cirrhosis, Biliary - physiopathology</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Lymphocyte Activation</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Other diseases. Semiology</subject><subject>Phytohemagglutinins - pharmacology</subject><subject>T-Lymphocytes - drug effects</subject><subject>T-Lymphocytes - metabolism</subject><subject>T-Lymphocytes - physiology</subject><issn>0270-9139</issn><issn>1527-3350</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><recordid>eNqFkLtOAzEQRS0ECiHQ0iG5QHQb_NqHSwSBIEWCItQrxxkrhn3h2RCl4xP4Rr6EjRIROqorzT1zZ3QJOedsyBkT1wtohjxTjCdMcXlA-jwWaSRlzA5Jn4mURZpLfUxOEF8ZY1qJrEd63ShTWveJuwPnrYeqpb5qIRSwfPPV9-eXoAGwqSv0H1ABIq0dndJiXTaL2q5bQOpCXdLGtJtlpCvfLmgTfGnCms584TdqfQiLGj2ekiNnCoSznQ7Iy_1oejuOJk8Pj7c3k8hKoWQUx5pbnoCRSerAzYSOEwNZalMphNWpFYl1mdHpbO7YHCRnMjEutpxLkSmbyAG52uY2oX5fArZ56dFCUZgK6iXmXY5UKhEdONyCNtSIAVy--z3nLN8Um3fF5vtiu4WLXfJyVsJ8j2-b7PzLnW_QmsIFU1mPv5hSSqYi6zC9xVa-gPU_R_Px6PnPCz-4c5P8</recordid><startdate>199210</startdate><enddate>199210</enddate><creator>Menéndez, José Luis</creator><creator>Girón, José Antonio</creator><creator>Manzano, Luis</creator><creator>Garrido, Aurelio</creator><creator>Abreu, Luis</creator><creator>Albillos, Agustin</creator><creator>Durántez, Alberto</creator><creator>Alvarez‐Mon, Melchor</creator><general>W.B. 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Abdomen</topic><topic>Humans</topic><topic>Interleukin-2 - biosynthesis</topic><topic>Interleukin-2 - pharmacology</topic><topic>Liver Cirrhosis, Biliary - pathology</topic><topic>Liver Cirrhosis, Biliary - physiopathology</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Lymphocyte Activation</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Other diseases. Semiology</topic><topic>Phytohemagglutinins - pharmacology</topic><topic>T-Lymphocytes - drug effects</topic><topic>T-Lymphocytes - metabolism</topic><topic>T-Lymphocytes - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Menéndez, José Luis</creatorcontrib><creatorcontrib>Girón, José Antonio</creatorcontrib><creatorcontrib>Manzano, Luis</creatorcontrib><creatorcontrib>Garrido, Aurelio</creatorcontrib><creatorcontrib>Abreu, Luis</creatorcontrib><creatorcontrib>Albillos, Agustin</creatorcontrib><creatorcontrib>Durántez, Alberto</creatorcontrib><creatorcontrib>Alvarez‐Mon, Melchor</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>Hepatology (Baltimore, Md.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Menéndez, José Luis</au><au>Girón, José Antonio</au><au>Manzano, Luis</au><au>Garrido, Aurelio</au><au>Abreu, Luis</au><au>Albillos, Agustin</au><au>Durántez, Alberto</au><au>Alvarez‐Mon, Melchor</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Deficient interleukin‐2 responsiveness of T lymphocytes from patients with primary biliary cirrhosis</atitle><jtitle>Hepatology (Baltimore, Md.)</jtitle><addtitle>Hepatology</addtitle><date>1992-10</date><risdate>1992</risdate><volume>16</volume><issue>4</issue><spage>931</spage><epage>936</epage><pages>931-936</pages><issn>0270-9139</issn><eissn>1527-3350</eissn><coden>HPTLD9</coden><abstract>There is increasing evidence that primary biliary cirrhosis is associated with an alteration of the immune system. Although the cause remains unknown, it has been suggested that the immune system of patients with primary biliary cirrhosis is involved in the pathogenesis of their disease. We have investigated the T‐cell function in patients with primary biliary cirrhosis and have found defective phytohemagglutinin‐induced T‐cell mitogenesis. Likewise, their blastogenic response to CD3 monoclonal antibody was also depressed, although the DNA synthesis induced by stimulation with phorbol esters (12‐O‐tetradecanoilphorbol‐13‐acetate) plus ionophore (ionomycin) was normal. These alterations could not be ascribed either to a decreased synthesis of interleukin‐2 or to a defective expression of interleukin‐2 receptor after cellular activation. Moreover, this defective proliferative response of T lymphocytes was observed even in the presence of saturating concentrations of exogenous interleukin‐2. These results represent evidence of the deficiency in the interleukin‐2—dependent pathway found in T lymphocytes from patients with primary biliary cirrhosis. (HEPATOLOGY 1992;16:931–936.)</abstract><cop>Philadelphia, PA</cop><pub>W.B. Saunders</pub><pmid>1398499</pmid><doi>10.1002/hep.1840160413</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Biological and medical sciences Cell Division - drug effects Gastroenterology. Liver. Pancreas. Abdomen Humans Interleukin-2 - biosynthesis Interleukin-2 - pharmacology Liver Cirrhosis, Biliary - pathology Liver Cirrhosis, Biliary - physiopathology Liver. Biliary tract. Portal circulation. Exocrine pancreas Lymphocyte Activation Medical sciences Middle Aged Other diseases. Semiology Phytohemagglutinins - pharmacology T-Lymphocytes - drug effects T-Lymphocytes - metabolism T-Lymphocytes - physiology |
title | Deficient interleukin‐2 responsiveness of T lymphocytes from patients with primary biliary cirrhosis |
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