Immunosuppressive effects of apoptotic cells

Voll, Reinhard; Herrmann, Martin; Roth, Edith; Stach, C.; Kalden, Joachim R.; Girkontaitė, Irutė

doi:10.1038/37022

Cited by 1,635 publications

(1,338 citation statements)

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“…The loss of intestinal intraepithelial and lamina propria lymphocytes might facilitate bacterial translocation into the systemic circulation, thereby perpetuating the systemic inflammatory response and predisposing to secondary infections. The detrimental effects of apoptosis are not only associated with the severe loss of immune cells but also with the effect that apoptotic cell uptake has on surviving immune cells 16. The uptake of apoptotic cells by monocytes, macrophages, and DC results in immune tolerance by inducing anergy or a T helper 2 cell‐associated immune phenotype with increased IL‐10 production 17…”

Section: Mechanism Of Sepsis‐induced Immunosuppressionmentioning

confidence: 99%

Mechanisms of sepsis‐induced immunosuppression and immunological modification therapies for sepsis

Ono

Tsujimoto

Hiraki

et al. 2018

Annals of Gastroent Surgery

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Surgical injury can be a life‐threatening complication, not only due to the injury itself, but also due to immune responses to the injury and subsequent development of infections, which readily result in sepsis. Sepsis remains the leading cause of death in most intensive care units. Unfavorable outcomes of several high‐profile trials in the treatment of sepsis have led researchers to state that sepsis studies need a new direction. The immune response that occurs during sepsis is characterized by a cytokine‐mediated hyper‐inflammatory phase, which most patients survive, and a subsequent immunosuppressive phase. Therefore, therapies that improve host immunity might increase the survival of patients with sepsis. Many mechanisms are responsible for sepsis‐induced immunosuppression, including apoptosis of immune cells, increased regulatory T cells and expression of programmed cell death 1 on CD4+ T cells, and cellular exhaustion. Immunomodulatory molecules that were recently identified include interleukin‐7, interleukin‐15, and anti‐programmed cell death 1. Recent studies suggest that immunoadjuvant therapy is the next major advance in sepsis treatment.

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Section: Mechanism Of Sepsis‐induced Immunosuppressionmentioning

confidence: 99%

Mechanisms of sepsis‐induced immunosuppression and immunological modification therapies for sepsis

Ono

Tsujimoto

Hiraki

et al. 2018

Annals of Gastroent Surgery

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“…One pathway, however, involves CD36-TSP-1 interaction, and reminiscent of what occurs in endothelial cells, this interaction can interrupt another signal-in this case a lipopolysaccharide (LPS) induced pro-inflammatory cascade (Voll, Herrmann, Roth, Stach, Kalden, & Girkontaite, 1997). The details of these events are yet to be elucidated, but the result is secretion of IL-10, an anti-inflammatory cytokine, and inhibition of secretion of the pro-inflammatory cytokines TNF-α, IL-12 and IL-1β.…”

Section: Cd36 Signalingmentioning

confidence: 99%

“…CD36 uptake of apoptotic cells was shown to be one pathway in the suppression of pro-inflammatory cytokines (Voll, Herrmann, Roth, Stach, Kalden, & Girkontaite, 1997), and CD36 is up-regulated in response to IL-4 , a TH2 cytokine, and down regulated by LPS , Memon, Feingold, Moser, Fuller, & Grunfeld, 1998. Foam cell formation, however, has hallmarks of both a pro-inflammatory (TH1) and innate, scavenger receptor (TH2) phenotype.…”

Section: Other Functions Of Cd36 That May Impact Cardiovascular Diseasementioning

confidence: 99%

CD36: Implications in cardiovascular disease

Febbraio

Silverstein

2007

The International Journal of Biochemistry & Cell Biology

215

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CD36 is a broadly expressed membrane glycoprotein that acts as a facilitator of fatty acid uptake, a signaling molecule, and a receptor for a wide range of ligands, including apoptotic cells, modified forms of low density lipoprotein, thrombospondins, fibrillar beta-amyloid, components of gram positive bacterial walls and malaria infected erythrocytes. CD36 expression on macrophages, dendritic and endothelial cells, and in tissues including muscle, heart, and fat, suggest diverse roles, and indeed, this is truly a multifunctional receptor involved in both homeostatic and pathologic conditions. Despite an impressive increase in our knowledge of CD36 functions, in depth understanding of the mechanistic aspects of this protein remains elusive. This review focuses on CD36 in cardiovascular disease-what we know, and what we have yet to learn.

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“…However, it becomes more and more clear that apoptotic cellassociated molecular patterns can signal "safety" to the phagocyte. Exposure of PS is the best-characterized flag resulting in an antiinflammatory clearance of apoptotic cells (2,3,29,63) without induction of an immune response (10). Many other molecules may await discovery in the near future.…”

Section: Resultsmentioning

confidence: 99%

“…The two major mechanisms of cell death are apoptosis and primary necrosis. In contrast to necrotic cells, apoptotic ones maintain their membrane integrity and are usually cleared by macrophages via a noninflammatory pathway (2,3).…”

Section: Disposal Of Dying Cells: a Balancing Act Between Infection Amentioning

confidence: 99%