Interleukin-10 inhibits endotoxin-induced pro-inflammatory cytokines in microglial cell cultures

Kremlev, Sergey G.; Palmer, Charles

doi:10.1016/j.jneuroim.2005.01.010

Cited by 112 publications

(83 citation statements)

References 72 publications

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“…IL-10, a pleiotropic TH 2 cytokine, has obvious suppressive effects on the production of pro-inflammatory cytokines by monocytes-macrophages and inhibits the expression of activating molecules on these cells and dendrite cells [38,39]. Kremlev demonstrated that IL-10 has protected LPS-induced microglial cell death in in vivo and in in vitro study [39].…”

Section: Discussionmentioning

confidence: 99%

Apelin activates the expression of inflammatory cytokines in microglial BV2 cells via PI-3K/Akt and MEK/Erk pathways

Chen

Tao

Jiang

2015

Sci. China Life Sci.

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Section: Discussionmentioning

confidence: 99%

Apelin activates the expression of inflammatory cytokines in microglial BV2 cells via PI-3K/Akt and MEK/Erk pathways

Chen

Tao

Jiang

2015

Sci. China Life Sci.

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“…CNS IL-10 expression correlates with disease resolution (46). The critical role for IL-10 in the modulation of EAE is not surprising considering the potent activity of this cytokine in subduing activated macrophage and glial cells that play crucial effector roles in the disease (47,48). Nevertheless, it provides evidence that iTreg and nTreg operate through similar mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Mitigation of Experimental Allergic Encephalomyelitis by TGF-β Induced Foxp3+ Regulatory T Lymphocytes through the Induction of Anergy and Infectious Tolerance

Selvaraj

Geiger

2008

The Journal of Immunology

109

107

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Stimulation of naive T lymphocytes in the presence of IL-2 and TGF-β induces the regulatory transcription factor Foxp3, which endows the cells with regulatory functions. To better understand the properties and therapeutic potential of these induced regulatory T cells (iTreg), we examined their immunomodulatory properties in myelin oligodendroglial glycoprotein-induced experimental allergic encephalomyelitis (MOG-EAE). Adoptively transferred iTreg were as potent as natural Foxp3+ Treg in preventing EAE development, and were active both prophylactically and after priming. The iTreg migrated into the CNS in quantity, skewing the ratio of regulatory to effector T lymphocytes. IL-10−/− iTreg failed to suppress disease, demonstrating a critical role for iTreg IL-10 production in their therapeutic activity. MOG-specific T cells from iTreg treated animals were anergic. The cells failed to proliferate in response to Ag except in the presence of exogenous IL-2, and did not secrete or secreted reduced amounts of IL-2, IFN-γ, and IL-17. MOG-specific T cells were not wholly unresponsive though, as they did secrete IL-10 after stimulation. To determine whether iTreg-mediated tolerance was infectious, fostering the development of T lymphocytes that could independently suppress EAE, we purged draining lymph node cells from MOG-immunized, iTreg treated mice of the administered iTreg, and transferred the remaining cells to Ag-inexperienced mice. The transferred cells were able to block EAE development. Thus iTreg are highly potent suppressors of autoimmune encephalomyelitis, and act in an IL-10 dependent manner both through the induction of anergy in effector T cells and through the infectious induction of protective T lymphocytes able to independently suppress disease development.

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“…[40][41][42] Its neuroprotective characteristics include suppression of microglia and astroglia activation, as well as decreased production of proinflammatory cytokines 43,44 and reactive oxygen species. 45 Thus, it has been proposed that IL-10 treatment improves outcome in neuropathology.…”

Section: Interleukin-10mentioning

confidence: 99%

Involvement of Pro- and Anti-Inflammatory Cytokines and Chemokines in the Pathophysiology of Traumatic Brain Injury

2010

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Summary:Despite dramatic improvements in the management of traumatic brain injury (TBI), to date there is no effective treatment available to patients, and morbidity and mortality remain high. The damage to the brain occurs in two phases, the initial primary phase being the injury itself, which is irreversible and amenable only to preventive measures to minimize the extent of damage, followed by an ongoing secondary phase, which begins at the time of injury and continues in the ensuing days to weeks. This delayed phase leads to a variety of physiological, cellular, and molecular responses aimed at restoring the homeostasis of the damaged tissue, which, if not controlled, will lead to secondary insults. The development of secondary brain injury represents a window of opportunity in which pharmaceutical compounds with neuroprotective properties could be administered. To establish effective treatments for TBI victims, it is imperative that the complex molecular cascades contributing to secondary injury be fully elucidated. One pathway known to be activated in response to TBI is cellular and humoral inflammation. Neuroinflammation within the injured brain has long been considered to intensify the damage sustained following TBI. However, the accumulated findings from years of clinical and experimental research support the notion that the action of inflammation may differ in the acute and delayed phase after TBI, and that maintaining limited inflammation is essential for repair. This review addresses the role of several cytokines and chemokines following focal and diffuse TBI, as well as the controversies around the use of therapeutic anti-inflammatory treatments versus genetic deletion of cytokine expression.

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Interleukin-10 inhibits endotoxin-induced pro-inflammatory cytokines in microglial cell cultures

Cited by 112 publications

References 72 publications

Apelin activates the expression of inflammatory cytokines in microglial BV2 cells via PI-3K/Akt and MEK/Erk pathways

Apelin activates the expression of inflammatory cytokines in microglial BV2 cells via PI-3K/Akt and MEK/Erk pathways

Mitigation of Experimental Allergic Encephalomyelitis by TGF-β Induced Foxp3+ Regulatory T Lymphocytes through the Induction of Anergy and Infectious Tolerance

Involvement of Pro- and Anti-Inflammatory Cytokines and Chemokines in the Pathophysiology of Traumatic Brain Injury

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