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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Alternative splicing of myeloid IgA Fc receptor (Fc alpha R, CD89) transcripts in inflammatory responses.

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.[1]

References

  1. Alternative splicing of myeloid IgA Fc receptor (Fc alpha R, CD89) transcripts in inflammatory responses. Togo, S., Shimokawa, T., Fukuchi, Y., Ra, C. FEBS Lett. (2003) [Pubmed]
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