Circulating dendritic cells following burn

D’Arpa, N.; Accardo-Palumbo, Antonina; Amato, Giorgio; D’Amelio, L.; Pileri, D.; Cataldo, Vince D.; Mogavero, R.; Lombardo, Carla; Napoli, B.; Conte, Fábio F.

doi:10.1016/j.burns.2008.05.027

Cited by 42 publications

(27 citation statements)

References 15 publications

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“…One can speculate that activation of the inflammatory response through detection of pathogen-associated molecular patterns (PAMPs) and release of danger-associated molecular patterns [23] lead synergistically to profound DC depletion, whereas signals induced by recognition of PAMPs only have a modest effect on DC counts. Consistent with this hypothesis, a decrease in circulating DCs has been reported in infected burn patients, a clinical context in which infection and tissue damage coexist [24]. Alternatively, the loss of compartmentalization of the infection and the presence of overwhelming inflammation in the SS setting may contribute to activate molecular mechanisms that lead to the depletion of circulating DCs [25].…”

Section: Discussionmentioning

confidence: 72%

Profound and persistent decrease of circulating dendritic cells is associated with ICU-acquired infection in patients with septic shock

et al. 2011

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Section: Discussionmentioning

confidence: 72%

Profound and persistent decrease of circulating dendritic cells is associated with ICU-acquired infection in patients with septic shock

et al. 2011

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“…Phenotypic changes in the innate immune system, like impaired function of neutrophils (7), reductions in circulating dendritic cells (8), and increased production of immune-suppressive mediators like PGE 2 and nitric oxide (9) have been reported to occur in trauma patients. In addition, recent evidence suggests that CD4+ regulatory T cells (Tregs), which were originally identified as suppressors of CD4+ T cell activation (10), contribute to the counter-inflammatory reaction to severe injury (11).…”

Section: Introductionmentioning

confidence: 99%

Injury Induces Early Activation of T-Cell Receptor Signaling Pathways in CD4+ Regulatory T Cells

Hanschen¹,

Tajima²,

O’Leary³

et al. 2011

Shock

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Although it is known that injury enhances the regulatory activity of CD4+ regulatory T cells (Tregs), the cellular and molecular mechanisms responsible for injury-induced Treg activation remain unclear. This study was designed to investigate and compare injury-induced T cell receptor (TCR) signaling in Tregs, non-Tregs, and CD8+ T cells. Specifically, we used phospho-flow cytometry to measure the expression and phosphorylation of ZAP-70, PKC-θ, NFATc1, and GSK-3β in FoxP3+ Tregs vs. FoxP3-non-Tregs vs. CD8+ T cells. Groups of male, C57BL/6J mice underwent burn- or sham-injury and lymph nodes and spleens were harvested at early time points – 15, 30, 60, 120, and 240 minutes – to measure TCR signaling. As early as 15 minutes after burn injury, we observed a significant upregulation and phosphorylation of ZAP-70, PKC-θ, NFATc1, and GSK-3β in Tregs prepared from injury-site draining lymph nodes. Burn injury did not activate TCR signaling in Tregs from the spleen or in CD4+ non-Tregs and CD8+ T cells. In conclusion, the results of this study demonstrate that burn injury activates TCR signaling in Tregs, but not non-Tregs or CD8+ T cells. These findings suggest that injury provides an early TCR-activating signal to Tregs and supply new insights into how injury influences the adaptive immune system.

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“…To our knowledge, this is the first report to describe decreased blood myeloid DC subsets following vaccination in humans, however transient decreases in blood myeloid DCs have been observed in other conditions: 1) during acute myocardial infarction, where it is suggested that they are being recruited into the vessel wall and accumulating in atherosclerotic plaques (18–22), 2) in burn patients where it is associated with the incidence of sepsis (23), and 3) during acute viral infections including CMV (24) and pandemic H1N1 influenza (25). Additionally, following injection of the TLR7/8 agonist R-848 or the TLR9 agonist CpG-ODN in rhesus macaques, a decline in mDC were observed (26).…”

Section: Discussionmentioning

confidence: 88%

Transient decrease in human peripheral blood myeloid dendritic cells following influenza vaccination correlates with induction of serum antibody

Kobie

Treanor

Ritchlin

2014

Immunological Investigations

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Dendritic cells (DC) are critical inducers of the adaptive immune response. Extensive characterization of tissue-resident and monocyte-derived DC has revealed diverse stimulatory and regulatory actions, although the role of peripheral blood dendritic cells (PBDC) in maintaining homeostasis remains unclear. Examination of various myeloid (CD11c+CD303−) and plasmacytoid (CD11c−CD303+) DC populations in the peripheral blood of seasonal trivalent inactivated influenza vaccine recipients revealed a transient decrease in the frequency of CD11c+CD1c− myeloid DC subsets 5–10 days following vaccination, including both CD141+ and CD141− myeloid DC subsets of this population. These populations rebounded by 1 month, while plasmacytoid DC remained stable. The magnitude of the decrease in the CD141+ myeloid DC subset at d5–7 significantly correlated with the induction of influenza specific serum antibodies measured at 1 month following vaccination. These results demonstrate a mobilization of peripheral blood myeloid DC following vaccination and indicate these cells are potential biomarkers of immune response.

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Circulating dendritic cells following burn

Cited by 42 publications

References 15 publications

Profound and persistent decrease of circulating dendritic cells is associated with ICU-acquired infection in patients with septic shock

Profound and persistent decrease of circulating dendritic cells is associated with ICU-acquired infection in patients with septic shock

Injury Induces Early Activation of T-Cell Receptor Signaling Pathways in CD4+ Regulatory T Cells

Transient decrease in human peripheral blood myeloid dendritic cells following influenza vaccination correlates with induction of serum antibody

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