Le choix de J.-P. Sartre

Lehner, Frederick; Troisfontaines, Roger

doi:10.2307/40086445

Cited by 3 publications

(2 citation statements)

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“…Tapasin mediates complex formation and the crosstalk of structural information of MHC and TAP and is therefore important for class I assembly and editing. Tapasin has two independent functions: First, it increases the level of TAP, thereby increasing the e¤ciency of peptide transport and, secondly, it associates with MHC class I molecules, thereby facilitating directly loading and assembly of class I molecules [40,41]. The MHC-peptide complexes, which are kinetically stable, can leave the ER to the cell surface.…”

Section: Loading Of Peptides From Tap Onto Mhc Moleculesmentioning

confidence: 99%

The transporter associated with antigen processing TAP: structure and function

Lankat–Buttgereit

Tampé

1999

FEBS Letters

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The transport of antigenic peptides from the cytosol to the lumen of the endoplasmic reticulum (ER) is an essential process for presentation to cytotoxic T-lymphocytes. The transporter associated with antigen processing (TAP) is responsible for the intracellular translocation of peptides across the membrane of the ER. Efficient assembly of MHC-peptide complex requires the formation of a macromolecular transport and chaperone complex composed of TAP, tapasin and MHC class I molecules. Therefore, structure and function of TAP is important for the understanding of the immune surveillance.z 1999 Federation of European Biochemical Societies.

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Section: Loading Of Peptides From Tap Onto Mhc Moleculesmentioning

confidence: 99%

The transporter associated with antigen processing TAP: structure and function

Lankat–Buttgereit

Tampé

1999

FEBS Letters

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“…Antigen processing and presentation in the MHC class I pathway have not been studied in I: cruzi infection. MHC class I molecules are expressed on the surface of most nucleated cells and present peptides primarily derived from the cytoplasm to the immune system [32]. As T. cruzi is an intracellular pathogen that resides within the host cell cytoplasm [33], this localization suggests that proteins shed from T. cruzi are accessible to the MHC class I pathway for presentation to CD8+ lymphocytes, as has been shown for Listeria monocytogenes .…”

Section: Introductionmentioning

confidence: 99%

Trypanosoma cruzi infection does not impair major histocompatibility complex class I presentation of antigen to cytotoxic T lymphocytes

1997

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Trypanosoma cruzi (T. cruzi), the etiological agent of Chagas' disease, lives free within the cytoplasm of infected host cells. This intracellular niche suggests that parasite antigens may be processed and presented on major histocompatibility complex (MHC) class I molecules for recognition by CD8+ T cells. However, the parasite persists indefinitely in the mammalian host, indicating its success at evading immune clearance. It has been shown that T. cruzi interferes with processing and presentation of antigenic peptides in the MHC class II pathway. This investigation sought to determine whether interference in MHC class I processing and presentation occurs with T. cruzi infection. Surface expression of MHC class I molecules was found to be unaffected or up-regulated by T. cruzi infection in vitro. A model system employing a beta-galactosidase (beta-gal)-specific murine cytotoxic T lymphocyte (CTL) line (0805B) showed: (i) in vitro infection of mouse peritoneal macrophages or J774 cells with T. cruzi did not inhibit MHC class I presentation of exogenous peptide (a nine-amino acid epitope of beta-gal) to the CTL line, (ii) in vitro infection of a beta-gal-expressing 3T3 cell line (LZEJ) with T. cruzi did not inhibit MHC class I presentation of the endogenous protein to the CTL line and (iii) mouse renal adenocarcinoma cells infected with T. cruzi and subsequently infected with adenovirus expressing beta-gal were able to present antigen to the beta-gal-specific CTL line. These findings indicate that the failure of the immune response to clear T. cruzi does not result from global interference by the parasite with MHC class I processing and presentation. Parasites engineered to express beta-gal were unable to sensitize infected antigen-presenting cells in vitro to lysis by the CTL 0805B line. This was probably due to the intracellular localization of the beta-gal within the parasite and its inaccessibility to the host cell cytoplasm.

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Existentialism and Existence

Smith¹

1948

The Thomist

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Le choix de J.-P. Sartre

Cited by 3 publications

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The transporter associated with antigen processing TAP: structure and function

The transporter associated with antigen processing TAP: structure and function

Trypanosoma cruzi infection does not impair major histocompatibility complex class I presentation of antigen to cytotoxic T lymphocytes

Existentialism and Existence

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