Publication: Intrinsic antibody-dependent enhancement of microbial infection in macrophages: Disease regulation by immune complexes
Issued Date
2010-01-01
Resource Type
ISSN
14733099
Other identifier(s)
2-s2.0-77957160633
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
The Lancet Infectious Diseases. Vol.10, No.10 (2010), 712-722
Suggested Citation
Scott B. Halstead, Suresh Mahalingam, Mary A. Marovich, Sukathida Ubol, David M. Mosser Intrinsic antibody-dependent enhancement of microbial infection in macrophages: Disease regulation by immune complexes. The Lancet Infectious Diseases. Vol.10, No.10 (2010), 712-722. doi:10.1016/S1473-3099(10)70166-3 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/29875
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Intrinsic antibody-dependent enhancement of microbial infection in macrophages: Disease regulation by immune complexes
Abstract
A wide range of microorganisms can replicate in macrophages, and cell entry of these pathogens via non-neutralising IgG antibody complexes can result in increased intracellular infection through idiosyncratic Fcγ-receptor signalling. The activation of Fcγ receptors usually leads to phagocytosis. Paradoxically, the ligation of monocyte or macrophage Fcγ receptors by IgG immune complexes, rather than aiding host defences, can suppress innate immunity, increase production of interleukin 10, and bias T-helper-1 (Th1) responses to Th2 responses, leading to increased infectious output by infected cells. This intrinsic antibody-dependent enhancement (ADE) of infection modulates the severity of diseases as disparate as dengue haemorrhagic fever and leishmaniasis. Intrinsic ADE is distinct from extrinsic ADE, whereby complexes of infectious agents with non-neutralising antibodies lead to an increased number of infected cells. Intrinsic ADE might be involved in many protozoan, bacterial, and viral infections. We review insights into intracellular mechanisms and implications of enhanced pathogenesis after ligation of macrophage Fcγ receptors by infectious immune complexes. © 2010 Elsevier Ltd.