FceRI–FcgRII Coaggregation inhibits IL-16 production from human langerhans-like dendritic cells

UNCG Author/Contributor (non-UNCG co-authors, if there are any, appear on document)
Christopher Kepley, Associate Professor (Creator)
The University of North Carolina at Greensboro (UNCG )
Web Site: http://library.uncg.edu/

Abstract: Langerhans-like dendritic cells (LLDC) express the high-affinity IgE receptor FceRI form that lacks the ß-chain, and may play an important role in allergic inflammation via production of IL-16. Secretion of mediators by human mast cells and basophils is mediated through FceRI and is decreased by coaggregating these receptors to the low-affinity IgG receptor, FcgRII. We used a recently described human Ig fusion protein(GE2), which is composed of key portions of the human g1 and the human e heavy chains, to investigate its ability to inhibit IL-16 production from FceRI-positive Langerhans-like dendritic cells through coaggregation of FcgRII and FceRI. Unstimulated LLDC-derived from CD14-positive monocytes from atopic donors were shown to express FcgRII, an ITIM-containing receptor, but not FceRI or FcgRIII which are activating (ITAM) receptors. When passively sensitized with antigen-specific, human IgE and then challenged with antigen, LLDC were stimulated to produce IL-16. However, when FceRI and FcgRII were coaggregated with GE2, IL-16 production was significantly inhibited. Exposure of LLDCs to GE2 alone did not induce IL-16 production. Our results further extend our studies demonstrating the ability of GE2 to inhibit FceRI-mediated responses through coaggregation with FcgRIIB and at the same time show that human LDCC can be modulated in a fashion similar to mast cells and basophils.

Additional Information

Clinical Immunology 2003; 108:89-94.
Language: English
Date: 2003
Langerhans cell, Dendritic cells, IgE, Fc receptors, IL-16

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