Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/79963
Title: Fc gamma RIIIA negatively impacts humoral immune responses but not overall lung inflammation in an ovalbumin-induced allergic asthma mouse model
Authors: Zhou, PP
Wu, TQ
Jin, XQ
Li, J
Yan, HJ
Zhou, L
Huang, YL
Wang, J
Zhou, HY
Zhu, XP
Zou, X 
Fang, Y
Keywords: Fc gamma receptor
Fc gamma RIIIA
Allergic asthma
Airway inflammation
Allergy
Issue Date: 2018
Publisher: Karger
Source: International archives of allergy and immunology, 2018, v. 176, no. 1, p. 61-73 How to cite?
Journal: International archives of allergy and immunology 
Abstract: Background: Fc gamma receptors (Fc gamma R) play substantial immune regulatory roles both positively and negatively in pathophysiological processes including allergy and asthma. Compared with Fc gamma RIIB which is classically defined as an inhibitory receptor, mouse Fc gamma RIIIA and its functional human homologue Fc gamma RIIA have been assumed to be activating receptors. However, evidence demonstrating inhibitory regulation by mouse Fc gamma RIIIA has recently been emerging.
Objective: To dissect the contributory roles of mouse Fc gamma RIIIA (human Fc gamma RIIA) in parallel with Fc gamma RIIB in an ovalbumin (OVA)-induced mouse model of asthma and to preliminarily assess the correlation of the respective Fc gamma R with circulating IgE levels in human asthma patients.
Methods: Wild-type, Fc gamma RIIB-/-, and Fc gamma RIIIA(-/-) mice were used in an OVA-induced asthma model followed by assessment of the allergic pathology focused on the lung tissues. Expression levels of Fc gamma RIIB, Fc gamma RIIA, and Fc gamma RIIIA on peripheral blood mononuclear cells (PBMC) together with the circulating IgE levels in the serum from patients with allergic asthma were analysed.
Results: Although enhanced humoral immune responses typically represented by augmented OVA-specific IgG and IgE levels in serum were observed in the absence of Fc gamma RIIIA in the mouse asthma model, no overall regulation by Fc gamma RIIIA, especially in terms of those parameters measuring lung tissue inflammation, was recorded. As expected, in the absence of Fc gamma RIIB, augmented immune responses measured as serum antibody levels as well as those in various regulatory pathways in this mouse asthma model were observed. The expression levels of human Fc gamma RIIB but not Fc gamma RIIA were negatively correlated with serum levels of IgE in human asthma patients.
Conclusion: We did not find major evidence demonstrating an immune inhibitory role of mouse Fc gamma RIIIA in this OVA-induced mouse asthma model. As asthma is a complex disease and the immune regulatory responses involve sophisticated components and pathways, the exact roles of Fc gamma RIIIA as well as its human functional homologue Fc gamma RIIA in asthma still await further clarification using other mouse asthma models as well as clinical studies.
URI: http://hdl.handle.net/10397/79963
ISSN: 1018-2438
EISSN: 1423-0097
DOI: 10.1159/000487539
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