Literature DB >> 14598254

Distinct costimulation dependent and independent autoreactive T-cell clones in primary biliary cirrhosis.

Takashi Kamihira1, Shinji Shimoda, Kenichi Harada, Akira Kawano, Mizuki Handa, Eishi Baba, Koichi Tsuneyama, Minoru Nakamura, Hiromi Ishibashi, Yasuni Nakanuma, M Eric Gershwin, Mine Harada.   

Abstract

BACKGROUND & AIMS: Previous work has suggested that CD4+ CD28- or costimulation-independent T cells are increased in autoimmune diseases. In this study, we compared frequency and qualitative characteristics of autoreactive costimulation-independent or CD4+ CD28- T cells in primary biliary cirrhosis (PBC) by taking advantage of the well-defined immunodominant autoepitope of the E2 component of pyruvate dehydrogenase (PDC-E2).
METHODS: We determined the frequency of costimulation-independent autoreactive T cells that respond to PDC-E2 163-176 and the frequency of CD4+ CD28- T cells. Finally, we determined the role of biliary epithelial cells (BEC) as both an antigen-presenting cell or, alternatively, as a target cell for T-cell-mediated cytotoxicity.
RESULTS: The precursor frequency of costimulation-independent CD4+ T cells that respond to PDC-E2 163-176 and the frequency of CD4+ CD28- T cells were dramatically elevated in PBC. Furthermore, 2 types of T-cell clones that respond to PDC-E2 163-176 emerged from this study. One type was costimulation dependent and the other costimulation independent. Both types of clones lyse BEC in a similar effector target (E/T) ratio distribution. However, BEC did not help the proliferation of any T-cell clones. Furthermore, costimulation-independent T-cell clones do not become anergic by BEC.
CONCLUSIONS: In PBC, costimulation-independent autoreactive T cells, which do not become anergic, increase and maintain the autoimmune response. In controls, although autoantigens are expressed on BEC and autoantigen-reactive T cells exist around BEC, autoantigen-reactive T cells are costimulation dependent and will become anergic and maintain peripheral tolerance.

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Year:  2003        PMID: 14598254     DOI: 10.1016/j.gastro.2003.07.013

Source DB:  PubMed          Journal:  Gastroenterology        ISSN: 0016-5085            Impact factor:   22.682


  21 in total

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2.  Augmented expression of hepatocytes growth factor activator inhibitor type 1 (HAI-1) in intrahepatic small bile ducts in primary biliary cirrhosis.

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Review 4.  Primary biliary cirrhosis: what do autoantibodies tell us?

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5.  Plasma cells and the chronic nonsuppurative destructive cholangitis of primary biliary cirrhosis.

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6.  Periductal interleukin-17 production in association with biliary innate immunity contributes to the pathogenesis of cholangiopathy in primary biliary cirrhosis.

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7.  Biliary epithelial apoptosis, autophagy, and senescence in primary biliary cirrhosis.

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8.  WAVE3 Induces EMT and Promotes Migration and Invasion in Intrahepatic Cholangiocarcinoma.

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9.  B cell depletion in treating primary biliary cirrhosis: pros and cons.

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Review 10.  Lymphocyte recruitment and homing to the liver in primary biliary cirrhosis and primary sclerosing cholangitis.

Authors:  Andrea T Borchers; Shinji Shimoda; Christopher Bowlus; Carl L Keen; M Eric Gershwin
Journal:  Semin Immunopathol       Date:  2009-06-17       Impact factor: 9.623

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