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. 2014 Mar 22;11:54. doi: 10.1186/1742-2094-11-54

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Copyright © 2014 St-Amour et al.; licensee 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 credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Modulation of the fractalkine pathway by IVIg treatment: correlation with cortical Aβ42/Aβ40 ratios and Aβ*56. Expression of CX3CR1 was evaluated using flow cytometry in the bone marrow of 3xTg-AD mice treated with IVIg from 9 to 12 months. Decreases in the percentage of CX3CR1⁺ cells in (A) total bone marrow cells and (B) the monocyte population were observed in treated animals (n = 11 to 12). (C) The percentage of CX3CR1⁺ cells in the bone marrow correlated with soluble and insoluble Aβ42/Aβ40 ratios (in IVIg-treated mice) and Aβ*56 concentrations from the parietotemporal cortex (in control and total animals). Statistical analysis: (A,B) one-way ANOVA with Tukey’s multiple comparison test. *P <0.05. (C) Correlations were determined by simple linear regression analysis. 3xTg-AD, triple-transgenic mouse model of Alzheimer’s disease; ANOVA, analysis of variance; IVIg, human intravenous immunoglobulin.