Martin E, Boucher C, Fontaine B, Delarasse C. Distinct inflammatory phenotypes of microglia and monocyte-derived macrophages in Alzheimer's disease models: effects of aging and amyloid pathology. Aging Cell. 2017 Feb;16(1):27-38. Epub 2016 Oct 8 PubMed.
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University of Zurich
This is a very interesting study that shows the potential of flow-cytometry-based studies in the AD field. I was pleased to see that many of our observations (Ferretti et al., 2016) /papers/t-cell-brain-infiltration-and-immature-antigen-presenting-cells-transgenic-models-alzheimers have been confirmed by Dr. Martin et al. In particular, we also observed lack of MHC-II upregulation on “invading macrophages” in aged APP mice. (The nature of these CD45high CD11β-positive cells is still very enigmatic, as they might be invading macrophages as well as perivascular, resident macrophages). We also found that in spite of being more numerous (as the authors here report), MHC-II-positive microglial cells had lower levels of surface MHC-II than WT counterparts. Together these results might highlight impaired antigen presentation. Furthermore, it is clear from figure 1A and B that aged APP-tg mice harbor an increased population of lymphocytes (CD450-positive, CD11β-negative), as we have shown. It would be interesting to further characterise this population in the context of raging and amyloidosis.
References:
Ferretti MT, Merlini M, Späni C, Gericke C, Schweizer N, Enzmann G, Engelhardt B, Kulic L, Suter T, Nitsch RM. T-cell brain infiltration and immature antigen-presenting cells in transgenic models of Alzheimer's disease-like cerebral amyloidosis. Brain Behav Immun. 2016 May;54:211-25. Epub 2016 Feb 9 PubMed.
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