Ischemia‐induced neuronal expression of the microglia attracting chemokine secondary lymphoid‐tissue chemokine (SLC)

Biber, Knut; Sauter, André; Brouwer, Nieske; Copray, Sjef; Boddeke, Hendrikus

doi:10.1002/glia.1047

Cited by 127 publications

(154 citation statements)

References 51 publications

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“…Recently, we have described the induction of CCL21 expression in ischemic mouse neurons and the effects of CCL21 in microglia, suggesting the involvement of CCL21 in the communication between damaged neurons and microglia (11)(12)(13). Surprisingly, murine microglia responded to CCL21 stimulation in the absence of CCR7 via the alternative receptor CXCR3 (13)(14)(15), confirming results previously obtained in a recombinant expression system (5).…”

supporting

confidence: 86%

Cutting Edge: Activity of Human Adult Microglia in Response to CC Chemokine Ligand 21

Dijkstra

Hulshof

Valk

et al. 2004

The Journal of Immunology

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The approximately 50 known chemokines are classified in distinct subfamilies: CXC, CC, CX3C, and C. Although the signaling of chemokines often is promiscuous, signaling events between members of these distinct chemokine classes are hardly observed. The only known exception so far is the murine CC chemokine ligand (CCL)21 (secondary lymphoid tissue chemokine, Exodus-2, 6Ckine), which binds and activates the murine CXC chemokine receptor CXCR3. However, this exception has not been found in humans. In this study, we provide evidence that human CCL21 is a functional ligand for endogenously expressed CXCR3 in human adult microglia. In absence of CCR7 expression, CCL21 induced chemotaxis of human microglia with efficiency similar to the CXCR3 ligands CXC chemokine ligand 9 (monokine induced by IFN-γ) and CXC chemokine ligand 10 (IFN-γ-inducible protein-10). Because human CCL21 did not show any effects in CXCR3-transfected HEK293 cells, it is indicated that CXCR3 signaling depends on the cellular background in which the CXCR3 is expressed.

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supporting

confidence: 86%

Cutting Edge: Activity of Human Adult Microglia in Response to CC Chemokine Ligand 21

Dijkstra

Hulshof

Valk

et al. 2004

The Journal of Immunology

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“…Repeated immunization of plt/plt mice may increase production of IL-6 and TGF-␤, thereby contributing to further generation of Th17 cells and development of EAE (9,11,12). Alternatively, stimulation with CXCL9, CXCL10, and/or CXCL11 via CXCR3, an additional receptor for mouse CCL21 (25)(26)(27), might partially substitute for CCR7 stimulation in heavily immunized plt/plt or CCR7 Ϫ/Ϫ mice. These possibilities might also explain why DLN cells from plt/plt mice produced a small but detectable amount of IL-17 (Fig.…”

Section: Discussionmentioning

confidence: 99%

CCR 7 Ligands Are Required for Development of Experimental Autoimmune Encephalomyelitis through Generating IL-23-Dependent Th17 Cells

Kuwabara¹,

Ishikawa²,

Yasuda³

et al. 2009

The Journal of Immunology

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CCL19 and CCL21 are thought to be critical for experimental autoimmune encephalomyelitis (EAE) induction, but their precise role is unknown. We examined the role of these chemokines in inducing EAE. C57BL/6 mice lacking expression of these chemokines (plt/plt mice) or their receptor CCR7 were resistant to EAE induced with myelin oligodendrocyte glycoprotein peptide 35–55 (MOG35–55) and pertussis toxin. However, passive transfer of pathogenic T cells from wild-type mice induced EAE in plt/plt mice, suggesting a defect independent of the role of CCR7 ligands in the migration of immune cells. Examination of draining lymph node (DLN) cells from MOG35–55-immunized plt/plt mice found decreased IL-23 and IL-12 production by plt/plt dendritic cells (DCs) and a concomitant defect in Th17 cell and Th1 cell generation. In contrast, production of the Th17 lineage commitment factors IL-6 and TGF-β were unaffected by loss of CCR7 ligands. The adoptive transfer of in vitro-generated Th17 cells from DLN cells of MOG35–55-immunized plt/plt mice developed EAE in wild-type recipient mice, whereas that of Th1 cells did not. Pathogenic Th17 cell generation was restored in plt/plt DLNs with the addition of exogenous IL-23 or CCL19/CCL21 and could be reversed by inclusion of anti-IL-23 mAb in cultures. Exogenous CCL19/CCL21 induced IL-23p19 expression and IL-23 production by plt/plt or wild-type DCs. Therefore, CCR7 ligands have a novel function in stimulating DCs to produce IL-23 and are important in the IL-23-dependent generation of pathogenic Th17 cells in EAE induction.

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“…Endangered neurons can release proinflammatory chemokines such as monocyte chemoattractant protein-1 (MCP-1/CCL2) and secondary lymphoid-tissue chemokine (SLC/CCL21). Expression of MCP-1 and SLC is increased in neurons after ischemia [29,30]. Subsequently, recruited and activated microglial cells produce inflammatory mediators, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and nitric oxide (NO), which contribute to delayed neuronal death [31].…”

Section: Discussionmentioning

confidence: 99%

Delayed neuronal cell death in brainstem after transient brainstem ischemia in gerbils

et al. 2010

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Background Because of the lack of reproducible brainstem ischemia models in rodents, the temporal profile of ischemic lesions in the brainstem after transient brainstem ischemia has not been evaluated intensively. Previously, we produced a reproducible brainstem ischemia model of Mongolian gerbils. Here, we showed the temporal profile of ischemic lesions after transient brainstem ischemia. Results Brainstem ischemia was produced by occlusion of the bilateral vertebral arteries just before their entry into the transverse foramina of the cervical vertebrae of Mongolian gerbils. Animals were subjected to brainstem ischemia for 15 min, and then reperfused for 0 d (just after ischemia), 1 d, 3 d and 7 d (n = 4 in each group). Sham-operated animals (n = 4) were used as control. After deep anesthesia, the gerbils were perfused with fixative for immunohistochemical investigation. Ischemic lesions were detected by immunostaining for microtubule-associated protein 2 (MAP2). Just after 15-min brainstem ischemia, ischemic lesions were detected in the lateral vestibular nucleus and the ventral part of the spinal trigeminal nucleus, and these ischemic lesions disappeared one day after reperfusion in all animals examined. However, 3 days and 7 days after reperfusion, ischemic lesions appeared again and clusters of ionized calcium-binding adapter molecule-1(IBA-1)-positive cells were detected in the same areas in all animals. Conclusion These results suggest that delayed neuronal cell death took place in the brainstem after transient brainstem ischemia in gerbils.

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Ischemia‐induced neuronal expression of the microglia attracting chemokine secondary lymphoid‐tissue chemokine (SLC)

Cited by 127 publications

References 51 publications

Cutting Edge: Activity of Human Adult Microglia in Response to CC Chemokine Ligand 21

Cutting Edge: Activity of Human Adult Microglia in Response to CC Chemokine Ligand 21

CCR 7 Ligands Are Required for Development of Experimental Autoimmune Encephalomyelitis through Generating IL-23-Dependent Th17 Cells

Delayed neuronal cell death in brainstem after transient brainstem ischemia in gerbils

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