Novel insights for high mobility group box 1 protein-mediated cellular immune response in sepsis:A systemic review

Astragaloside IV attenuates inflammatory reaction via activating immune function of regulatory T-cells inhibited by HMGB1 in mice

“…A growing number of studies still focus on the inflammation-regulatory function and its contribution to infectious and inflammatory disorders, recent data suggest that HMGB1 formation can also markedly influence the host cellmediated immunity, including neutrophils, dendritic cells and macrophages (Zhao et al 2012;Zhu et al, 2012). In addition, our study has also illustrated the potential role of HMGB1 in regulating splenic Tregs and the influence on T-cell-mediated immunity in mice (Huang et al 2012). With the discovery of HMGB1 as a potent mediator of inflammation and the presence of extranuclear HMGB1 in several inflammatory conditions, possible beneficial effects of HMGB1-targeted therapies have been investigated.…”

“…However, the interaction between HMGB1 and Tregs has not been made clear, thus the effects of HMGB1 on the immune function of Tregs and its potential mechanism are worth investigating. Our recent experiment showed that HMGB1 stimulation resulted in significantly down-regulation of expression of Tregs cell phenotypes in vitro (Huang et al 2012). Our present study was performed to identify the effect of HMGB1 on splenic CD4 þ CD25 þ Tregs in mice in vivo, and to determine the mechanism underlying immune dysfunction related to HMGB1 stimulation, aiming at looking for a possible measure to prevent the development of sepsis following severe acute insults.…”

Association between HMGB1 and asthma: a literature review

“…In particular IL-4Rα, a subunit in cognate receptors with IL-4, activate signal transducer and transcription of factor-6 (STAT-6), important for IL-4 release from antigen-stimulated, which play a predominant role in the immune system [36, 37]. …”

“…In fact, as illustrated in Fig. 1 , recent studies have shown the interaction of HMGB1 with RAGE, TLR2, and TLR4 that transduces intracellular signals that activate protein kinases (MAPKs) and nuclear factor kappaB (NF-kB), which lead to the activation and the release of pro-inflammatory cytokines (e.g., TNF and Interleukins) [ 36 , 37 ].

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Ketamine reduces LPS-induced HMGB1 via activation of the Nrf2/HO-1 pathway and NF-κB suppression

“…There must be many possibilities; one reason is probably LPS-induced inflammatory mediators' release by activating many signaling pathways, NF-JB pathways are commonly one of them. 5,39 Our studies only demonstrates that ketamine inhibits LPS-induced HMGB1 release by inhibiting NF-JB signaling; whether ketamine inhibits HMGB1-induced proinflammatory cytokines release by inhibiting NF-JB signaling needs to be further explored. HMGB1 was implicated as a ''late'' mediator of lethal systemic inflammation in sepsis.…”