Type II activation of macrophages and microglia by immune complexes enhances Th17 biasing in an IL-6-independent manner

Sarrabeth Stone, Anne Camille La Flamme

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3 Scopus citations


Macrophages can be activated into several distinct activation states. One of these states, type II activation, has a regulatory phenotype characterized by decreased IL-12 and increased IL-10, and has been shown to bias naïve CD4+ T cells to a Th2 response. Microglia, the resident macrophage-like cells in the central nervous system (CNS), are important contributors to neuroinflammation and, thus, we investigated if type II activated microglia could bias CD4+ T cell responses in a similar manner as type II activated macrophages. Using immune complex ligation in the presence of LPS to induce type II activation, we found that both type II macrophages and type II microglia biased CD4+ T cell responses in vitro to express increased levels of IL-17A and CD124. The enhanced IL-17A production occurred independently of IL-6, and IL-10 and IL-12, which were key regulators of IFN-γ production, but were not involved in the increased IL-17A. Finally, we found that another type II-activating compound, glatiramer acetate, did not bias CD4+ T cells to produce enhanced IL-17A. Taken together, this study demonstrates that microglia can be type II activated and, similarly to type II macrophages, can bias CD4+ T cell responses; however, depending on the type II stimulus, the effect on CD4+ T cell subset differentiation may vary.

Original languageEnglish (US)
Article numbere0164454
JournalPloS one
Issue number10
StatePublished - Oct 2016

Bibliographical note

Funding Information:
This work was funded by the Neurological Foundation of New Zealand (1029-PG to ACL) and New Zealand Lottery Grants Board (to SS).

Publisher Copyright:
© 2016 Stone, La Flamme. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


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