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As the spines mature, ICAM-5 migrates away from the postsynaptic density to the spine shafts.

Microglia express integrins that have been shown to bind ICAM-5 in other cells (Akiyama and Mc Geer, 1990).These phagocytic cells remove excess synapses through a process that is regulated by components of the complement cascade (Stevens et al., 2007; Schafer et al., 2012).If ICAM-5 is bound to microglia, it could potentially regulate several aspects of the above-mentioned microglia functions.ICAM-5 further reduced the secretion of the proinflammatory cytokines tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β), but on the contrary induced the secretion of the anti-inflammatory IL-10 from lipopolysaccharide (LPS) stimulated microglia.Thus, ICAM-5 might be involved in the regulation of microglia in both health and disease, playing an important neuroprotective role when the brain is under immune challenges and as a “don’t-eat-me” signal when it is solubilized from active synapses.

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