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Chunk #0 — Background

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Neuroinflammation and M2 microglia: the good, the bad, and the inflamed.
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For the better part of a century, the function of microglia in the central nervous system (CNS) was a topic wrapped in controversy. Originally identified by Franz Nissl in 1899 as ‘Stabchenzellen’ or rod-like cells, and further classified by Pío del Río Hortega in 1919, these cells were determined to be a distinct non-neural and non-astrocytic population [1]. Furthermore, Hortega’s observations suggested a capacity for phagocytosis, indicating that these cells were more than just space filler or connective cells between neurons. Not all shared Hortega’s ideas. This included his mentor, the father of modern neuroscience, Ramón y Cajal, who urged Hortega not to publish and subsequently fired Hortega [2]. This early turmoil set the tone for decades to follow, during which the topics of microglial functions and origins were extensively debated [3]. However, beginning in the early 1980s, newer technology and ideas began to reveal the true nature of microglia as the brain’s resident immune cell. Even though we are starting to understand what microglia are capable of, many questions still remain. In particular, there is much to be learned about the plastic nature of these cells and the functions served by different microglial phenotypes.