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Microglia Homeostasis

During non-pathological conditions, microglia must be kept in a quiescent, non-inflamed state in order to maintain normal homeostasis. Specific control mechanisms exist in the local environment that actively prevent microglia from adopting an inflammatory profile. Healthy neurons express multiple surface ligands that interact with respective proteins on neighboring microglia to regulate activation of the glial cells. For example, neuronal CX3CL1/Fractalkine and CD200 interact with microglia CX3CR1 and CD200 R1, respectively. CX3CR1 and CD200 R1 are ITIM (immunoreceptor tyrosine-based inhibitory) immunoreceptors that suppress downstream immune signaling. Soluble factors released by nearby cells will also maintain microglia in an immune-suppressed state. For instance, neuronal-derived neurotrophic factors, such as Brain-Derived Neurotrophic Factor (BDNF) and Nerve Growth Factor (beta-NGF), inhibit the expression of MHC class II and co-stimulatory molecules on microglial cells. Additionally, neurotransmitters and neuropeptides, such as GABA and dopamine, suppress the production of proinflammatory cytokines. Microglia activation following injury or diseases is initiated, in part, with the loss of these inhibitory signals. R&D Systems offers a range of research tools needed for the investigation of microglia activation.