Fig. 3From: Understanding immune microenvironment alterations in the brain to improve the diagnosis and treatment of diverse brain diseasesTherapeutic targets for brain disorders Inhibition of P2X7R and activation of TREM2 can promote the transition of microglia to the M2 subtype. miRNA-124 inhibits PU.1-induced microglial proliferation by reducing the synthesis of C/EBP-α. CCR2 is a target for reducing the recruitment of CD4+ T cells to the brain. IFN-γ secreted by CD4 + T cells can induce the activation of the M1 subset, while IFN-β promotes the activation of M2 and B cells and increases the levels of CCL3 and CCL5, which are responsible for immature DC recruitment. CYBB/NOX2, which can improve the antigen presentation capability of DCs, is another target for an excessive immune response and can be inhibited by gene depletion or antibody neutralization. Anti-CD20 antibodies can reduce the number of T-bet+ B cells induced by IFN-γ. BTKis can also inhibit the function of B cells by inhibiting mitochondrial respiration and thus reduce the activation of T cells. The α5 integrin is a target for reducing the recruitment and infiltration of monocytes in the CNS. Created with BioRender.comBack to article page