Loss of Sprouty4 in T cells ameliorates experimental autoimmune encephalomyelitis in mice by negatively regulating IL-1β receptor expression

Fukaya, Takao; Someya, Kazue; Hibino, Sana; Okada, Masahiro; Yamane, Hitomi; Taniguchi, Koji; Yoshimura, Akihiko

doi:10.1016/j.bbrc.2014.04.012

Cited by 7 publications

(10 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, spry4-/-mice exhibited delayed onset and less severe experimental allergic encephalomyelitis (EAE) symptoms compared to wildtype mice (Fukaya et al, 2014). Our results suggest that endogenous activation of tyrosine kinase receptor signalling in spry4-/-mice is able to reduce inflammation to similar extent as exhibited following Fgf2 injections in wildtype mice.…”

Section: Discussionsupporting

confidence: 53%

Decreased anti-regenerative effects after spinal cord injury in spry4−/− mice

et al. 2015

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 53%

Decreased anti-regenerative effects after spinal cord injury in spry4−/− mice

et al. 2015

View full text Add to dashboard Cite

“…Not surprisingly, IL-1R expression was severely impaired in T H cells lacking STAT3, the primary transcription factor downstream of IL-6 receptor signaling. Recent reports have identified three novel T H 17 cell-intrinsic positive regulators of IL-1R expression, including the signaling regulator Spry4 (84), microRNA cluster miR-183-96-182 (85), and IL-1R signaling itself (64). Fukaya et al found that Spry4-deficient mice were partially resistant to active EAE and that T H 17 cells from these mice were unable to elicit passive EAE (84).…”

Section: Il-1β Acts On Th Cells To Promote Pathogenicity In Eaementioning

confidence: 99%

“…Recent reports have identified three novel T H 17 cell-intrinsic positive regulators of IL-1R expression, including the signaling regulator Spry4 (84), microRNA cluster miR-183-96-182 (85), and IL-1R signaling itself (64). Fukaya et al found that Spry4-deficient mice were partially resistant to active EAE and that T H 17 cells from these mice were unable to elicit passive EAE (84). Spry4-deficient T H 17 cells expressed lower levels of IL-1R, and overexpression of Spry4 increased expression of the Il1r1 transcript.…”

Section: Il-1β Acts On Th Cells To Promote Pathogenicity In Eaementioning

confidence: 99%

New Insights into the Role of IL-1β in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis

Lin

Edelson

2017

The Journal of Immunology

121

View full text Add to dashboard Cite

Multiple sclerosis, and its animal model experimental autoimmune encephalomyelitis, are neuroinflammatory diseases driven by autoreactive pathogenic TH cells which elicit demyelination and axonal damage. How TH cells acquire pathogenicity and communicate with myeloid cells and cells of the central nervous system remain unclear. IL-1β is recognized to play an important role in EAE and perhaps MS. Clinical EAE is significantly attenuated in IL-1 receptor-deficient and IL-1β-deficient mice, and IL-1β is found in the blood, cerebrospinal fluid, and CNS lesions of MS patients. Here, we will focus on new reports which elucidate the cellular sources of IL-1β and its actions during EAE, in both lymphoid tissues and within the CNS. Several immune cell types serve as critical producers of IL-1β during EAE, with the cytokine inducing responses in hematopoietic and non-hematopoietic cells. These findings from the EAE model should inspire efforts towards investigating the therapeutic potential of IL-1 blockade in MS.

show abstract

“…Further mechanistic studies using targeted deletion of IL-1R1 in astrocytes, given its importance not only in Th17 differentiation (40,41), or with the IL-1β neutralizing antibody Canakinumab (42) may provide a deeper understanding of the role of IL-1β signaling in astrocytes and might point to novel cell-type specific strategies with a potential role in treating late stage disease.…”

Section: Role Of Selected Pro- and Anti-inflammatory Cytokinesmentioning

confidence: 99%

Control of autoimmune CNS inflammation by astrocytes

2015

View full text Add to dashboard Cite

Multiple Sclerosis is a neurologic disease caused by immune cell infiltration into the central nervous system, resulting in grey and white matter inflammation, progressive demyelination and neuronal loss. Astrocytes, the most abundant cell population in the CNS, have been considered inert scaffold- or housekeeping cells for many years. However, recently it has become clear that this cell population actively modulates the immune response in the CNS at multiple levels. While being exposed to a plethora of cytokines during ongoing autoimmune inflammation, astrocytes modulate local CNS inflammation by secreting cytokines and chemokines, among other factors. This review article gives an overview of the most recent understanding about cytokine networks operational in astrocytes during autoimmune neuroinflammation and highlights potential targets for immunomodulatory therapies for Multiple Sclerosis.

show abstract

Loss of Sprouty4 in T cells ameliorates experimental autoimmune encephalomyelitis in mice by negatively regulating IL-1β receptor expression

Cited by 7 publications

References 29 publications

Decreased anti-regenerative effects after spinal cord injury in spry4−/− mice

Decreased anti-regenerative effects after spinal cord injury in spry4−/− mice

New Insights into the Role of IL-1β in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis

Control of autoimmune CNS inflammation by astrocytes

Contact Info

Product

Resources

About