In response to infectious pathogens, injurious protein aggregates (e.g., Aβ, α-synuclein, mutant huntingtin, prions) or tumor cells, microglia can initiate a neuroinflammatory response (Hickman et al., 2018). Profound morphological and molecular changes accompany microglial activation (figure 1) (Pinto et al., 2020). Upon stimulation, microglia retract and thicken processes evolving from a ramified state, to an intermediate 'bushy' state and finally converting to an amoeboid state (Yang et al., 2016; Pinto et al. 2020) (figure 2). Microglia activation leads to increased expression of IBA-1, MHCII, CD68 and CD11b, also known as integrin alpha M (ITGAM) (Pinto et al., 2020, Jurga et al., 2020). CD11b expression in microglia is induced in response to Nitric Oxide (NO) produced by the inducible nitric-oxide synthase iNOS (Roy et al., 2006). Together with CD18, also named integrin beta chain-2 (ITGB2), CD11b forms the integrin complement receptor 3 (CR3), which is involved in adhesion processes, phagocytic elimination of pathogens, induction of both inflammatory and tolerogenic responses, and modulation of parallel or downstream host defense pathways (Jurga et al., 2020; Lamers et al., 2021). CR3 expression is not restricted to microglial cells, but also found in neutrophils and other myeloid cells, including macrophages, monocytes and eosinophils (Lamers et al., 2021).