From: Dysregulated dendritic cells in sepsis: functional impairment and regulated cell death
Strategies | Treatment | Major functions | References |
---|---|---|---|
Modifying functions of DCs | Glucocorticoids | Reducing the production of IL-12 and augmenting the loss of CD8+ DCs | |
Thymosin α1 | Enhancing the expression of DCs surface molecules; upregulating the expression of TLR2 and TLR9 on the surface of DCs; promoting the secretion of IL-2, IL-12, and IFN-α | ||
TLR4 antagonist FP7 and Eritoran | Inhibiting cytokines storm and glycolysis reprogramming of DCs | ||
TLR2-derived peptides | Upregulating CD14 activity and promoting antigen-mediated DCs maturation; increasing the release of IL-12 and IFN-γ and decreasing the release of TNF-β; promoting the differentiation of T cells toward Th1 | ||
PLA2 | Increasing the expression of surface molecules of DCs and promoting DC maturation | ||
Anti-HMGB1 antibody | Augmenting maturation of DCs and T cell polarization toward Th1 | ||
Anti-C5a antibody | Enhancing IL-12+ DCs in the abdominal cavity and inhibiting them in peripheral blood and lymph nodes | ||
Inhibiting cell death of DCs | Silencing of miR-142-p, miR155, and miR-146a/b | Inhibiting the apoptosis of DCs; increasing production of proinflammatory cytokines such as IL-12p70, IL-6, TNF-α, and IFN-γ | |
Overexpressed VIM | Inhibiting apoptosis of DCs Inhibiting production of proinflammatory cytokines such as IL-2, IL-10, and IFN-α | [195] | |
Dexmedetomidine | Inhibiting the apoptosis of DCs; downregulating the production of sepsis-induced inflammatory mediators, including TNF-α and IL-6 |