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Fig. 3 | Cell Communication and Signaling

Fig. 3

From: Understanding immune microenvironment alterations in the brain to improve the diagnosis and treatment of diverse brain diseases

Fig. 3

Therapeutic 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.com

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