Neuroinflammation, and, to the same degree, all inflammation, is a fundamental immune response designed to protect the body from harm, arising from both endogenous and exogenous sources. Being the sentinel immune cell of the brain, microglia are tasked as the first responders to infection or tissue injury and initiating an inflammatory response. Using a full array of immune receptors, such as toll-like receptors (TLRs), nucleotide-binding oligomerization domains (NODs), NOD-like receptors, and many scavenger receptors [10,11], microglia (as well as other CNS cells, such as astrocytes) are able to recognize harmful stimuli and respond by producing inflammatory cytokines such as TNFα, IL-6, IL-1β, interferon-γ (IFNγ), and several chemokines [12]. This cytokine production is essential for the polarization of microglia into what has been termed a classically activated, ‘M1’, state [13]. This term parallels the Th1 terminology used for T cells, and underscores the close relationship between T cells and macrophages in the periphery. Interferon-γ produced from Th1 cells was found to be instrumental in polarizing macrophages to M1 [14]. However, the ability to produce these cytokines does not rest solely with
