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Thymosin‐α1 regulates MHC class I expression in FRTL‐5 cells at transcriptional level
Author(s) -
Giuliani Cesidio,
Napolitano Giorgio,
Mastino Antonio,
Di Vincenzo Simonetta,
D'Agostini Cartesio,
Grelli Sandro,
Bucci Ines,
Singer Dinah S.,
Kohn Leonard D.,
Monaco Fabrizio,
Garaci Enrico,
Favalli Cartesio
Publication year - 2000
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/1521-4141(200003)30:3<778::aid-immu778>3.0.co;2-i
Subject(s) - biology , microbiology and biotechnology , mhc class i , major histocompatibility complex , transfection , chloramphenicol acetyltransferase , reporter gene , gene expression , thymosin , enhancer , gene , electrophoretic mobility shift assay , flow cytometry , mhc class ii , genetics , immunology
Abstract In this study we examined the effect of the synthetic peptide thymosin‐α1 (Tα1) on MHC class I expression in FRTL‐5 cells. Treatment with Tα1 increased expression of MHC class I surface molecules and mRNA, which reached its peak (153 ± 8 % of the control value) after 12 h. Chloramphenicol acetyltransferase (CAT) analysis, following transfection with a plasmid containing the regulatory sequence of MHC class I (or its deletion derivatives) with the CAT reporter gene, and electrophoretic mobility shift assay experiments demonstrated that the action of Tα1 was at the transcriptional level, and its mechanism of action is likely due to increased binding between the complex p50 / fra‐2 and the enhancer A sequence of the 5' flanking region of a swine class I gene (PD1). An increase in the expression of MHC class I surface molecules was also observed by flow cytometry in murine and human tumor cell lines and in primary cultures of human macrophages. This study shows for the first time an effect of Tα1 on the regulation of gene expression at the molecular level, and may further contribute to explaining the results obtained using Tα1 in the control of infectious diseases and tumor growth.

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