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- W4313382148 abstract "Abstract Although the salience of the immune system in multiple sclerosis (MS) pathology has been established, the mechanisms and mediators involved are incompletely characterized. We have identified IL-15, which aids in the development, activation, and survival of immune cells, as a relevant contributor to MS neuropathology. We previously showed that greater proportions of myeloid cells, including peripheral monocytes and brain macrophages/microglia, from MS patients express IL-15 versus controls. Thus, we aim to identify the factors that contribute to these elevated IL-15 levels in the context of MS. Primary human monocytes from MS patients and age/sex matched healthy donors are treated with M-CSF to trigger differentiation into macrophages (considered M0 macrophages) prior to being polarized into M1 or M2 macrophages. While a small proportion of M0 macrophages express IL-15, M2 polarization significantly enhances the percentage of IL-15+ macrophages. In contrast, M1 polarization does not affect IL-15 levels although it significantly increases MHCI and CD80 expression. GM-CSF is produced by pathogenic encephalitogenic T cells; monocytes and macrophages express the corresponding receptor (GM-CSF receptor). GM-CSF induces a major increase in the proportion of IL-15+ M0 and M2 macrophages from both donor groups. In contrast, GM-CSF does not modify IL-15 expression by monocytes although it induces STAT5 phosphorylation. In conclusion, GM-CSF is a potent trigger for IL-15 expression on M0/M2 macrophages but not monocytes. Moreover, M2 polarization of macrophages increases IL-15 expression. Identification of IL-15 triggers and further characterization of IL-15+ immune cells may provide novel targets for therapies for MS patients." @default.
- W4313382148 created "2023-01-06" @default.
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- W4313382148 date "2017-05-01" @default.
- W4313382148 modified "2023-10-03" @default.
- W4313382148 title "GM-CSF upregulates IL-15 expression on specific human myeloid cells." @default.
- W4313382148 doi "https://doi.org/10.4049/jimmunol.198.supp.201.3" @default.
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