Isotype-specific regulation of MHC class II gene expression in human monocytes by exogenous and endogenous tumor necrosis factor
Autor: | Jerzy Wieckiewicz, Marek Zembala, Irena Ruggiero, Anna Pituch-Noworolska, Marek Jasiński |
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Rok vydání: | 1995 |
Předmět: |
Lipopolysaccharides
medicine.drug_class Genes MHC Class II Immunology Biology Monoclonal antibody medicine.disease_cause Monocytes Receptors Tumor Necrosis Factor MHC Class II Gene Autoimmunity Gene expression medicine Humans Immunology and Allergy RNA Messenger Cells Cultured HLA-D Antigens MHC class II Tumor Necrosis Factor-alpha Monocyte Antibodies Monoclonal HLA-DR Antigens Isotype Molecular biology Thalidomide Up-Regulation medicine.anatomical_structure Gene Expression Regulation biology.protein Tumor necrosis factor alpha |
Zdroj: | Journal of Clinical Immunology. 15:185-193 |
ISSN: | 1573-2592 0271-9142 |
DOI: | 10.1007/bf01541088 |
Popis: | The control of expression of MHC class II molecules on antigen-presenting cells is important for the induction of immunity, while aberrant expression of these molecules plays a role in the immunopathology of autoimmune diseases. This study explored the role of tumor necrosis factor alpha (TNF) in controlling the level of HLA class II mRNA in human monocytes. Exposure of monocytes to exogenous recombinant TNF (rTNF) selectively up-regulated DR alpha-mRNA but not DP or DQ alpha-mRNA. Inhibitors of TNF synthesis, pentoxifylline (PTX) and thalidomide, inhibited TNF mRNA accumulation in LPS-activated monocytes and down-regulated DR mRNA but not DP or DQ mRNA. The inhibitory effect of anti-TNF monoclonal antibody (MAb) indicated that endogenously generated TNF acted extracellularly. Anti-p75 TNF-R2 receptor and to a lesser extent anti-p55 TNF-R1 MAbs inhibited TNF-mediated up-regulation of DR mRNA and TNF mRNA. Taken together, this implies that endogenously generated TNF plays a role in controlling isotype-specific MHC class II gene expression in human monocytes/macrophages. These results may have some implications for anti-tumor response and autoimmunity. |
Databáze: | OpenAIRE |
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