Abstract
More than 10 splice variants of the Fc receptor for IgA (Fc alpha R, CD89) have been identified in human myeloid cells. In this study, we quantified Fc alpha R splice transcripts Delta EC2 and Delta 66 EC2, which lack the entire and a part of the homologous immunoglobulin-like extracellular domain 2 (EC2), respectively. Tumor necrosis factor-alpha was found to specifically increase the ratio of Delta EC2 to the wild type CD89 in neutrophils and conversely decrease the Delta EC2 ratio in monocytes. We also observed a significant decrease in the neutrophil Delta EC2/CD89 ratio in pneumonia patients. These results suggest that Delta EC2 is differentially regulated and could be involved in immunoregulation of IgA-mediated host defense.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Alternative Splicing / drug effects
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Alternative Splicing / genetics*
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Alternative Splicing / immunology*
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Antigens, CD / biosynthesis
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Antigens, CD / genetics*
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Antigens, CD / immunology*
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Humans
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Monocytes / drug effects
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Monocytes / immunology
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Myeloid Cells / drug effects
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Myeloid Cells / immunology
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Myeloid Cells / metabolism
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Neutrophils / drug effects
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Neutrophils / immunology
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Pneumonia / immunology*
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RNA, Messenger / metabolism
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Receptors, Fc / biosynthesis
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Receptors, Fc / genetics*
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Receptors, Fc / immunology*
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Reverse Transcriptase Polymerase Chain Reaction
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Tetradecanoylphorbol Acetate / pharmacology
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Tumor Necrosis Factor-alpha / pharmacology
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U937 Cells
Substances
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Antigens, CD
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Fc(alpha) receptor
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RNA, Messenger
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Receptors, Fc
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Tumor Necrosis Factor-alpha
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Tetradecanoylphorbol Acetate