当前位置： SCI文献检索 > INTERNATIONAL IMMUNOPHARMACOLOGY期刊下所有文献 > Low-affinity IgE receptor (FcepsilonRII)-mediated activation of human monocytes by both monomeric IgE and IgE/anti-IgE immune complex.

Low-affinity IgE receptor (FcepsilonRII)-mediated activation of human monocytes by both monomeric IgE and IgE/anti-IgE immune complex.

Abstract：

:Monocytes and macrophages of individuals with allergic diseases express increased levels of the low-affinity IgE receptors (FcepsilonRII or CD23) on their surfaces. The cross-linking of CD23-bound IgE antibody by allergen activates the cells to release inflammatory mediators. In mast cells, the binding of IgE to the high-affinity IgE receptors (FcepsilonRI) has recently been shown to activate these cells independent of allergen. It has not been determined if such is true of the binding of IgE to the low-affinity receptors. The purpose of this study was, therefore, to determine whether monomeric IgE alone can activate CD23-bearing human monocytes and how this may relate to the activation by IgE/anti-IgE immune complex. Purified monocytes, cultured for 48 h with IL-4 to up-regulate CD23 were sensitized with human myeloma IgE and further cultured for 24 h with or without anti-human IgE antibody. The release of cytokines TNF-alpha and MIP-1alpha (as an index of activation) was determined by enzyme immunoassay. Results showed that in IL-4-treated/CD23-bearing monocytes, sensitization with IgE alone caused a release of TNF-alpha and MIP-1alpha. The addition of anti-IgE antibody to cross-link the bound IgE resulted in the enhancement of the response. Such activation by monomeric IgE and IgE/anti-IgE immune complex was blocked with an anti-CD23 antibody, confirming the specific involvement of CD23 molecules. Neither of the activation modalities elevated intracellular cAMP, contrary to previous report. These results show for the first time, that in CD23-bearing monocytes, IgE sensitization alone can activate monocytes, and that ligation of such IgE by anti-IgE antibody only enhances the response. These observations have implications for the understanding of the pathophysiology of IgE-dependent inflammation accompanying many allergic diseases.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Ezeamuzie CI,Al-Attiyah R,Shihab PK,Al-Radwan R

doi

10.1016/j.intimp.2009.05.009

subject

Has Abstract

pub_date

2009-08-01 00:00:00

pages

1110-4

issue

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(09)00192-1

journal_volume

pub_type

杂志文章

在线工具

Low-affinity IgE receptor (FcepsilonRII)-mediated activation of human monocytes by both monomeric IgE and IgE/anti-IgE immune complex.