Retraction notice to “Myeloid-derived suppressor cells accumulate in the liver site after sepsis to induce immunosuppression” Cellular Immunology 279 (2012) 12–20

Ren, Dongping; Bi, Qing; Li, Li; Gao, Yongqiang; Li, Yingju; Liu, Jun; Li, Peng; Xiao, Jing

doi:10.1016/j.cellimm.2012.08.005

Cited by 10 publications

(5 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[127][128][129] Several studies also reported the migration and accumulation of MDSCs in spleen and liver during sepsis. 124,130 As sepsis is characterized by profound disturbances of the endothelium, we hypothesize that partial rupture of endothelial barrier in the bone marrow may contribute to the facilitated release of immature progenitors-this possibility requires further exploration.…”

Section: Myeloid-derived Suppressor Cellsmentioning

confidence: 99%

Myeloid cells in sepsis‐acquired immunodeficiency

Venet

Demaret

Gossez

et al. 2020

Annals of the New York Academy of Sciences

View full text Add to dashboard Cite

the World Health Organization recognized sepsis as a global health priority. Sepsis profoundly perturbs immune homeostasis by initiating a complex response that varies over time, with the concomitant occurrence of pro-and anti-inflammatory mechanisms. Sepsis deeply impacts myeloid cell response. Different mechanisms are at play, such as apoptosis, endotoxin tolerance, metabolic failure, epigenetic reprogramming, and central regulation. This induces systemic effects on circulating immune cells and impacts progenitors locally in lymphoid organs. In the bone marrow, a progressive shift toward the release of immature myeloid cells (including myeloid-derived suppressor cells), at the expense of mature neutrophils, takes place. Circulating dendritic cell number remains dramatically low and monocytes/macrophages display an anti-inflammatory phenotype and reduced antigen presentation capacity. Intensity and persistence of these alterations are associated with increased risk of deleterious outcomes in patients. Thus, myeloid cells dysfunctions play a prominent role in the occurrence of sepsis-acquired immunodeficiency. For the most immunosuppressed patients, this paves the way for clinical trials evaluating immunoadjuvant molecules (granulocyte-macrophage colony-stimulating factor and interferon gamma) aimed at restoring homeostatic myeloid cell response. Our review offers a summary of sepsis-induced myeloid cell dysfunctions and current therapeutic strategies proposed to target these defects in patients.

show abstract

Section: Myeloid-derived Suppressor Cellsmentioning

confidence: 99%

Myeloid cells in sepsis‐acquired immunodeficiency

Venet

Demaret

Gossez

et al. 2020

Annals of the New York Academy of Sciences

View full text Add to dashboard Cite

show abstract

“…The MDSCs of septic mice have a great potential to control inflammatory response and to protect the liver from injury induced by inflammation [60]. Liver MDSCs have a strong suppressive effect on CD4 + and CD8 + T cell proliferation via secreting arginase l and NO synthase 2.…”

Section: Liver Immune Response In Sepsismentioning

confidence: 99%

The Role of the Liver in Sepsis

Yan

2014

International Reviews of Immunology

418

352

View full text Add to dashboard Cite

Despite the progress made in the clinical management of sepsis, sepsis morbidity and mortality rates remain high. The inflammatory pathogenesis and organ injury leading to death from sepsis are not fully understood for vital organs, especially the liver. Only recently has the role of the liver in sepsis begun to be revealed. Pre-existing liver dysfunction is a risk factor for the progression of infection to sepsis. Liver dysfunction after sepsis is an independent risk factor for multiple organ dysfunction and sepsis-induced death. The liver works as a lymphoid organ in response to sepsis. Acting as a double-edged sword in sepsis, the liver-mediated immune response is responsible for clearing bacteria and toxins but also causes inflammation, immunosuppression, and organ damage. Attenuating liver injury and restoring liver function lowers morbidity and mortality rates in patients with sepsis. This review summarizes the central role of liver in the host immune response to sepsis and in clinical outcomes.

show abstract

“…Infection, especially that resulting in sepsis, is now known to lead to an expansion of MDSCs. Delano and colleagues originally identified a rapid and sustained increase in predominantly GR‐1 + CD11b + immature myeloid progenitors in the spleen, lymph nodes and bone marrow in a murine model of polymicrobial sepsis , a finding subsequently replicated multiple times . Indeed, the universal expansion of this population in nearly all inflammatory conditions has led to suggestions that it is a normal demand‐adapted component of the host response—‘emergency myelopoiesis’—as opposed to a pathological event .…”

Section: Specialized Regulatory Cell Phenotypesmentioning

confidence: 99%

“…In contrast, the ongoing survival and peripheral aggregation of MDSCs by an IL‐6‐stimulated gp130–STAT3 signalled release of acute‐phase proteins from hepatocytes was shown to be vital in controlling innate immunity and abrogated acute sepsis‐associated mortality in murine CLP . Adoptive transfer of sepsis‐induced hepatic MDSCs into normal mice has also been demonstrated to reduce early death from subsequent induction of acute hepatic failure by LPS and δ ‐galactosamine .…”

Section: Specialized Regulatory Cell Phenotypesmentioning

confidence: 99%

Pathways mediating resolution of inflammation: when enough is too much

2013

View full text Add to dashboard Cite

Patients with critical illness, and in particular sepsis, are now recognized to undergo unifying, pathogenic disturbances of immune function. Whilst scientific and therapeutic focus has traditionally been on understanding and modulating the initial pro-inflammatory limb, recent years have witnessed a refocusing on the development and importance of immunosuppressive 'anti-inflammatory' pathways. Several mechanisms are known to drive this phenomenon; however, no overriding conceptual framework justifies them. In this article we review the contribution of pro-resolution pathways to this phenotype, describing the observed immune alterations in terms of either a failure of resolution of inflammation or the persistence of pro-resolution processes causing inappropriate 'injurious resolution'-a novel hypothesis. The dysregulation of key processes in critical illness, including apoptosis of infiltrating neutrophils and their efferocytosis by macrophages, are discussed, along with the emerging role of specialized cell subtypes Gr1(+) CD11b(+) myeloid-derived suppressor cells and CD4(+) CD25(+) FoxP3(+) T-regulatory cells.

show abstract

Retraction notice to “Myeloid-derived suppressor cells accumulate in the liver site after sepsis to induce immunosuppression” Cellular Immunology 279 (2012) 12–20

Cited by 10 publications

References 28 publications

Myeloid cells in sepsis‐acquired immunodeficiency

Myeloid cells in sepsis‐acquired immunodeficiency

The Role of the Liver in Sepsis

Pathways mediating resolution of inflammation: when enough is too much

Contact Info

Product

Resources

About