A novel rat CC chemokine, identified by targeted differential display, is upregulated in brain inflammation

Utans-Schneitz, Ulrike; Lorez, H.P.; Klinkert, Wolfgang E. F.; Silva, Jean Da; Lesslauer, Werner

doi:10.1016/s0165-5728(98)00204-5

Cited by 31 publications

(16 citation statements)

References 56 publications

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“…Many leukocytes such as B cells, dendritic cells, CD4 ϩ T cells, and ␥-␦ T cells 57,58 express the LARC receptor, CCR6. Moreover, there is circumstantial evidence suggesting a role for LARC in inflammation, 57,59 but our findings would indicate that it is likely not involved in the active recruitment stage of granuloma formation. Because the source and target of LARC in granulomatous lungs is as yet unknown, it is difficult to speculate on its function.…”

Section: Discussionmentioning

confidence: 53%

Chemokine Expression Dynamics in Mycobacterial (Type-1) and Schistosomal (Type-2) Antigen-Elicited Pulmonary Granuloma Formation

Qiu

Frait

Reich

et al. 2001

The American Journal of Pathology

120

100

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Section: Discussionmentioning

confidence: 53%

Chemokine Expression Dynamics in Mycobacterial (Type-1) and Schistosomal (Type-2) Antigen-Elicited Pulmonary Granuloma Formation

Qiu

Frait

Reich

et al. 2001

The American Journal of Pathology

120

100

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“…Finally, we demonstrated that MIP-3␣ is required for sensitization of T cells to Ag and for release of T cells from lymph nodes during the course of an immune response. An increase in expression of MIP-3␣ in the spinal cord has previously been observed in PLP-induced EAE in the mouse (26) and in S100␤-and myelin oligodendrocyte glycoprotein-induced experimental autoimmune panencephalomyelitis in the rat (27). However, quantitation of MIP-3␣/CCL20 expression was not conducted in either of these previous studies.…”

Section: Discussionmentioning

confidence: 91%

A Role for Macrophage Inflammatory Protein-3α/CC Chemokine Ligand 20 in Immune Priming During T Cell-Mediated Inflammation of the Central Nervous System

Kohler

Caon

Willenborg

et al. 2003

The Journal of Immunology

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Chemokines are a family of cytokines that exhibit selective chemoattractant properties for target leukocytes and play a significant role in leukocyte migration. In this study, we have investigated the role of the C-C chemokine, macrophage inflammatory protein (MIP)-3α/CC chemokine ligand 20, in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), a model of T cell-dependent inflammation. Expression in the CNS of MIP-3α, as determined by RT-PCR, increased in a time-dependent manner such that peak expression correlated with peak clinical disease. Similarly, levels of immunoreactive MIP-3α in the draining lymph nodes increased up to 10-fold 9 days postimmunization and remained elevated for up to 21 days postimmunization. The increased production of MIP-3α coincided with onset of clinical disease. Treatment of mice with specific neutralizing anti-MIP-3α Abs significantly reduced the severity of both clinical EAE and neuroinflammation by inhibiting the sensitization of lymphocytes to the specific Ag and release of lymphocytes from the draining lymph nodes. In contrast, adoptive transfer experiments indicated that MIP-3α was not essential for the effector phase of EAE. Together, these data demonstrate that MIP-3α plays a critical role in the sensitization phase of EAE.

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“…CCL21 and its receptor in the ischemic CNS, CXCR3, were previously found to be induced in ischemic mouse brain (54)(55)(56). CXCR3-deficiency was associated with reduced microglial activity and reduced loss of secondary neurons in hippocampal formation in an entorhinal cortex lesion model (57).…”

Section: Discussionmentioning

confidence: 92%

CD93/AA4.1: A Novel Regulator of Inflammation in Murine Focal Cerebral Ischemia

Harhausen¹,

Prinz²,

Ziegler

et al. 2010

The Journal of Immunology

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International audienceThe stem-cell marker CD93 (AA4.1/C1qRp) has been described as a potential complement C1q-receptor. Its exact molecular function, however, remains unknown. By using global expression profiling we showed that CD93-mRNA is highly induced after transient focal cerebral ischemia. CD93 protein is upregulated in endothelial cells, but also in selected macrophages and microglia. To elucidate the potential functional role of CD93 in postischemic brain damage, we used mice with a targeted deletion of the CD93 gene. After 30 min of occlusion of the middle cerebral artery and 3 d of reperfusion these mice displayed increased leukocyte infiltration into the brain, increased edema, and significantly larger infarct volumes (60.8 ± 52.2 versus 23.9 ± 16.6 mm3) when compared with wild-type (WT) mice. When the MCA was occluded for 60 min, after 2 d of reperfusion the CD93 knockout mice still showed more leukocytes in the brain, but the infarct volumes were not different from those seen in WT animals. To further explore CD93-dependent signaling pathways, we determined global transcription profiles and compared CD93-deficient and WT mice at various time points after induction of focal cerebral ischemia. We found a highly significant upregulation of the chemokine CCL21/Exodus-2 in untreated and treated CD93-deficient mice at all time points. Induction of CCL21 mRNA and protein was confirmed by PCR and immunohistochemistry. CCL21, which was formerly shown to be released by damaged neurons and to activate microglia, contributes to neurodegeneration. Thus, we speculate that CD93-neuroprotection is mediated via suppression of the neuroinflammatory response through downregulation of CCL21

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A novel rat CC chemokine, identified by targeted differential display, is upregulated in brain inflammation

Cited by 31 publications

References 56 publications

Chemokine Expression Dynamics in Mycobacterial (Type-1) and Schistosomal (Type-2) Antigen-Elicited Pulmonary Granuloma Formation

Chemokine Expression Dynamics in Mycobacterial (Type-1) and Schistosomal (Type-2) Antigen-Elicited Pulmonary Granuloma Formation

A Role for Macrophage Inflammatory Protein-3α/CC Chemokine Ligand 20 in Immune Priming During T Cell-Mediated Inflammation of the Central Nervous System

CD93/AA4.1: A Novel Regulator of Inflammation in Murine Focal Cerebral Ischemia

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