Adoptive transfer of CD8+ T cells from transforming growth factor beta receptor type II (dominant negative form) induces autoimmune cholangitis in mice

Hepatology

Volumn 47, Issue 6, 2008, Pages 1974-1982

  Yang, Guo Xiang ^a   Lian, Zhe Xiong ^a,h   Chuang, Ya Hui ^a   Moritoki, Yuki ^a   Lan, Ruth Y ^a   Wakabayashi, Kanji ^a   Ansari, Aftab A ^b   Flavell, Richard A ^c   Ridgway, William M ^d   Coppel, Ross L ^e   Tsuneyama, Koichi ^f   Mackay, Ian R ^g   Gershwin, M Eric ^a,h  

^a UNIVERSITY OF CALIFORNIA   (United States)

^b EMORY UNIVERSITY SCHOOL OF MEDICINE   (United States)

^c YALE UNIVERSITY SCHOOL OF MEDICINE   (United States)

^d UNIVERSITY OF PITTSBURGH SCHOOL OF MEDICINE   (United States)

^e MONASH UNIVERSITY   (Australia)

^f UNIVERSITY OF TOYAMA   (Japan)

^g MONASH UNIVERSITY   (Australia)

^h UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

MITOCHONDRION ANTIBODY; RAG1 PROTEIN; TRANSFORMING GROWTH FACTOR BETA RECEPTOR 2; PROTEIN SERINE THREONINE KINASE; RECOMBINASE; TRANSFORMING GROWTH FACTOR BETA RECEPTOR; TRANSFORMING GROWTH FACTOR BETA TYPE II RECEPTOR; TRANSFORMING GROWTH FACTOR-BETA TYPE II RECEPTOR;

ADOPTIVE TRANSFER; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; AUTOIMMUNITY; CD4 LYMPHOCYTE COUNT; CD8+ T LYMPHOCYTE; CELL EXPANSION; CELL FUNCTION; CELL INFILTRATION; CHOLANGITIS; CONTROLLED STUDY; HISTOPATHOLOGY; MOUSE; NONHUMAN; PATHOGENESIS; PRIMARY BILIARY CIRRHOSIS; PRIORITY JOURNAL; ANIMAL; AUTOIMMUNE DISEASE; BILE DUCT; BILIARY CIRRHOSIS; C57BL MOUSE; CD4+ T LYMPHOCYTE; DISEASE MODEL; FEMALE; GENETICS; IMMUNOLOGY; LIVER; METABOLISM; MOUSE MUTANT; PATHOLOGY;

ADOPTIVE TRANSFER; ANIMALS; AUTOIMMUNE DISEASES; BILE DUCTS; CD4-POSITIVE T-LYMPHOCYTES; CD8-POSITIVE T-LYMPHOCYTES; CHOLANGITIS; DISEASE MODELS, ANIMAL; FEMALE; LIVER; LIVER CIRRHOSIS, BILIARY; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; PROTEIN-SERINE-THREONINE KINASES; RECEPTORS, TRANSFORMING GROWTH FACTOR BETA; RECOMBINASES;

EID: 46249110385     PISSN: 02709139     EISSN: None     Source Type: Journal    
DOI: 10.1002/hep.22226     Document Type: Article

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