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. 2011 Jul 31;14(9):1142-9.
doi: 10.1038/nn.2887.

Infiltrating monocytes trigger EAE progression, but do not contribute to the resident microglia pool

Bahareh Ajami  1 , Jami L Bennett, Charles Krieger, Kelly M McNagny, Fabio M V Rossi
Affiliations

Infiltrating monocytes trigger EAE progression, but do not contribute to the resident microglia pool

Bahareh Ajami et al. Nat Neurosci. .

Abstract

In multiple sclerosis and the experimental autoimmune encephalitis (EAE) mouse model, two pools of morphologically indistinguishable phagocytic cells, microglia and inflammatory macrophages, accrue from proliferating resident precursors and recruitment of blood-borne progenitors, respectively. Whether these cell types are functionally equivalent is hotly debated, but is challenging to address experimentally. Using a combination of parabiosis and myeloablation to replace circulating progenitors without affecting CNS-resident microglia, we found a strong correlation between monocyte infiltration and progression to the paralytic stage of EAE. Inhibition of chemokine receptor-dependent recruitment of monocytes to the CNS blocked EAE progression, suggesting that these infiltrating cells are essential for pathogenesis. Finally, we found that, although microglia can enter the cell cycle and return to quiescence following remission, recruited monocytes vanish, and therefore do not ultimately contribute to the resident microglial pool. In conclusion, we identified two distinct subsets of myelomonocytic cells with distinct roles in neuroinflammation and disease progression.

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References

    1. Nat Neurosci. 2007 Dec;10(12):1544-53 - PubMed
    1. J Neurosci Res. 1991 Feb;28(2):254-60 - PubMed
    1. Trends Neurosci. 1996 Aug;19(8):312-8 - PubMed
    1. Blood. 1997 Aug 1;90(3):986-93 - PubMed
    1. Clin Immunol Immunopathol. 1995 Oct;77(1):4-13 - PubMed

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