Interleukin-2 receptors and interleukin-2-mediated signaling in myelin: activation of diacylglycerol kinase and phosphatidylinositol 3-kinase

Chakraborty, Goutam; Drivas, A.; Ledeen, Robert W.

doi:10.1016/j.neuroscience.2003.09.003

Cited by 12 publications

(8 citation statements)

References 59 publications

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“…55 Up-regulation of CD25 has also been reported in the brain tissue of mice after lipopolysaccharide stimulation. 56 Furthermore, IL-2 can modulate the function and behavior of neurons, glia, and oligodendrocytes in vitro.…”

Section: Discussionmentioning

confidence: 97%

A Role for Natural Regulatory T Cells in the Pathogenesis of Experimental Cerebral Malaria

Amante

Stanley

Randall

et al. 2007

The American Journal of Pathology

160

172

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Section: Discussionmentioning

confidence: 97%

A Role for Natural Regulatory T Cells in the Pathogenesis of Experimental Cerebral Malaria

Amante

Stanley

Randall

et al. 2007

The American Journal of Pathology

160

172

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“…Oligodendrocytes express receptors to a wide range of mediators including IL‐4, IL‐6, IL‐7, IL‐10, IL‐11, IL‐12 and IL‐18. Expression of several of these is increased in neurological disorders . In addition, several chemokine receptors such as CXCR1, CXCR2 and CXCR3 are also expressed on oligodendrocytes at increased levels in MS, stroke and amyotrophic lateral sclerosis .…”

Section: Oligodendrocytes As Immune Targets and Immune Regulatorsmentioning

confidence: 99%

“…Expression of several of these is increased in neurological disorders. 68,69,86 In addition, several chemokine receptors such as CXCR1, CXCR2 and CXCR3 are also expressed on oligodendrocytes at increased levels in Antigen presentation and target for oligodendrocyte and/or myelin-specific T cells 60,61 Complement A range of complement factors and inhibitors expressed on oligodendrocytes have been described almost mainly restricted to cells in vitro. e.g.…”

Section: Oligodendrocytes As Immune Targets and Immune Regulatorsmentioning

confidence: 99%

Oligodendrocyte‐microglia cross‐talk in the central nervous system

et al. 2014

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Summary Communication between the immune system and the central nervous system (CNS) is exemplified by cross‐talk between glia and neurons shown to be essential for maintaining homeostasis. While microglia are actively modulated by neurons in the healthy brain, little is known about the cross‐talk between oligodendrocytes and microglia. Oligodendrocytes, the myelin‐forming cells in the CNS, are essential for the propagation of action potentials along axons, and additionally serve to support neurons by producing neurotrophic factors. In demyelinating diseases such as multiple sclerosis, oligodendrocytes are thought to be the victims. Here, we review evidence that oligodendrocytes also have strong immune functions, express a wide variety of innate immune receptors, and produce and respond to chemokines and cytokines that modulate immune responses in the CNS. We also review evidence that during stress events in the brain, oligodendrocytes can trigger a cascade of protective and regenerative responses, in addition to responses that elicit progressive neurodegeneration. Knowledge of the cross‐talk between microglia and oligodendrocytes may continue to uncover novel pathways of immune regulation in the brain that could be further exploited to control neuroinflammation and degeneration.

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“…PI-3 kinase has been reported to mediate IL-2-induced cell growth and survival, 4,[31][32][33] and recently cannabinoids were shown to inhibit ceramide-induced apoptosis in astrocytes through activation of PI-3 kinase. 34 As a mechanism by which PI-3 kinase induces inhibition of tumor necrosis factor-␣-induced apoptosis in primary astrocytes, PI-3 kinase-dependent inhibition of ceramide generation through SM hydrolysis was shown.…”

Section: Introductionmentioning

confidence: 99%

Interleukin-2-induced survival of natural killer (NK) cells involving phosphatidylinositol-3 kinase-dependent reduction of ceramide through acid sphingomyelinase, sphingomyelin synthase, and glucosylceramide synthase

Taguchi

Kondo

Watanabe

et al. 2004

Blood

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Interleukin 2 (IL-2) rescued human natural killer (NK) KHYG-1 cells from apoptosis along with a reduction of ceramide. Conversely, an increase of ceramide inhibited IL-2-rescued survival. IL-2 deprivation-induced activation of acid sphingomyelinase (SMase) and inhibition of glucosylceramide synthase (GCS) and sphingomyelin synthase (SMS) were normalized by IL-2 supplementation. A phosphatidyl inositol-3 (PI-3) kinase inhibitor, LY294002, inhibited IL-2-rescued survival, but a mitogen-activated protein kinase inhibitor, PD98059, and an inhibitor of Janus tyrosine kinase/signal transducer and activator of transcription pathway, AG490, did not. LY294002 inhibited IL-2-induced reduction of ceramide through activation of acid SMase and inhibition of GCS and SMS, suggesting the positive involvement of PI-3 kinase in ceramide reduction through enzymatic regulation. Indeed, a constitutively active PI-3 kinase enhanced growth rate and ceramide reduction through inhibition of acid SMase and activation of GCS and SMS. Further, LY294002 inhibited IL-2-induced changes of transcriptional level as well as mRNA and protein levels in acid SMase and GCS but did not affect the stability of the mRNAs. These results suggest that PI-3 kinase-dependent reduction of ceramide through regulation of acid SMase, GCS, and SMS plays a role in IL-2-rescued survival of NK cells. (Blood. 2004;104:3285-3293)

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Interleukin-2 receptors and interleukin-2-mediated signaling in myelin: activation of diacylglycerol kinase and phosphatidylinositol 3-kinase

Cited by 12 publications

References 59 publications

A Role for Natural Regulatory T Cells in the Pathogenesis of Experimental Cerebral Malaria

A Role for Natural Regulatory T Cells in the Pathogenesis of Experimental Cerebral Malaria

Oligodendrocyte‐microglia cross‐talk in the central nervous system

Interleukin-2-induced survival of natural killer (NK) cells involving phosphatidylinositol-3 kinase-dependent reduction of ceramide through acid sphingomyelinase, sphingomyelin synthase, and glucosylceramide synthase

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