Neuroinflammation describes the coordinated immune response of the central nervous system, driven principally by microglia and astrocytes, and it is increasingly recognized as an active contributor to virtually every neurodegenerative and neurological disorder. Microglia, the resident innate immune cells of the brain, are reliably identified by Iba1/AIF1, a calcium-binding protein upregulated upon activation, and by P2RY12, a purinergic receptor that marks homeostatic surveillant microglia and is downregulated as they adopt reactive states. Microglial survival and proliferation depend on signaling through CSF1R, the colony-stimulating factor 1 receptor, making it a key regulator of the resident myeloid population. TREM2 is a microglial surface receptor that senses lipids and damaged cells, promotes phagocytic clearance and metabolic fitness, and whose loss-of-function variants strongly increase the risk of Alzheimer's disease, underscoring the protective dimension of microglial activity. Phagocytic and lysosomal activity in reactive microglia and infiltrating macrophages is reflected by CD68. Inflammatory signaling is amplified by the NLRP3 inflammasome, a cytosolic sensor that assembles in response to danger signals to activate caspase-1 and drive maturation of interleukin-1 beta, linking innate sensing to chronic cytokine production. The classical complement cascade also participates in synapse elimination and inflammatory tagging, with Complement C1q initiating the pathway and marking synapses for removal by microglia. Astrocytes contribute through reactive gliosis, defined by upregulation of GFAP, the intermediate filament that forms the astrocytic cytoskeleton and is the canonical marker of astrocyte activation around lesions and degenerating tissue. Together these molecules profile the cellular identities and signaling events that define the inflamed CNS. This pack brings together validated antibodies against Iba1/AIF1, GFAP, CD68, TREM2, NLRP3, P2RY12, CSF1R, and Complement C1q to support detailed study of neuroinflammatory processes.
