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  • Meeting abstract
  • Open Access

Assessment of the immune-modulatory activity of sialylated fraction of IVIg in a murine model of allergic asthma

  • 1, 2,
  • 1,
  • 2,
  • 3 and
  • 1
Allergy, Asthma & Clinical Immunology20117 (Suppl 2) :A29

https://doi.org/10.1186/1710-1492-7-S2-A29

  • Published:

Keywords

  • Asthma
  • Dendritic Cell
  • Sialic Acid
  • Airway Inflammation
  • Treated Mouse

Background

Intravenous immunoglobulin (IVIg) has potent immune-modulating properties. In OVA-challenged mice, we demonstrated that IVIg markedly attenuates airway hyperresponsiveness (AHR) and abrogates airways inflammation, accompanied by substantial induction of antigen-specific Foxp3+ Treg from non-Treg precursors.

Methods

Mice were sensitized (i.n.) with OVA and then received IVIg or sialic acid enriched IVIg (SA-IVIg) fragments (i.p.), and then underwent challenge (i.n.). The induction of CD4+CD25+Foxp3+Treg was determined by flow-cytometry. AHR was measured, using a flexiVent small animal ventilator. Phenotypic properties of dendritic cells (DC) from various experimental groups were assessed by flow-cytometry. Expression of DCIR on DC was evaluated by flowcytometry and ICC. Adoptive transfer of DC was carried out to show the tolerogenic activity of IVIg-primed DC.

Results

IVIg and the SA-IVIg fraction induced Treg and abrogated AHR in OVA-challenged mice comparably. It followed by tolerogenic predisposition of DC (decrease of CD80/CD86 expression and IFN-γ production and increased level of IL-10). Adoptive transfer of DC from IVIg treated mice to OVA-challenged WT syngeneic mice has the similar anti-inflammatory activity of IVIg/SA-IVIg. Expression of DCIR (Inhibitory C-type lectin receptors) on DC of IVIg and SA-IVIg treated mice increased significantly.

Conclusions

IVIg induces Treg likely via conferring tolerogenic activities to DC. This mechanism is dependent on sialylated fraction of IVIg. DCIR is an inhibitory C-type lectin receptor that can be targeted by SA-IVIg and induce an inhibitory signal into the ligated cells. More dissection is required to confirming the role of DCIR in this model.

Authors’ Affiliations

(1)
Meakins-Christie Laboratories, McGill University, Montreal, QC, Canada, H2X 2P2
(2)
Département d’Immunologie et Microbiologie, Université de Montréal, Montreal, QC, Canada, H3C 3J7
(3)
Department of Microbiology and Immunology, McGill University Montreal, QC, Canada, H3G 1A4

Copyright

© Massoud et al; licensee BioMed Central Ltd. 2011

This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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