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Table 5 Putative role(s) of cytokines and chemokines that are increased in both human and mouse stroke

From: Multiplex immunoassay characterization and species comparison of inflammation in acute and non-acute ischemic infarcts in human and mouse brain tissue

Cytokine/chemokine Time-point Putative role Selected references
GM-CSF Acute Hematopoietic growth factor that plays a neuroprotective and angiogenic role in animal models of stroke. [33, 47]
IL12 (p70) Acute Sub-unit of the pro-inflammatory cytokine IL-12. Produced by antigen presenting cells. Co-factor for the polarization of T cells towards Th1 cell-mediated immunity. Role in animal models of stroke unknown. [50]
IP10 Acute Pro-inflammatory chemokine for monocytes and Th1 cells. Role in animal models of stroke unknown. [41]
KC/IL-8 Acute KC and IL-8 are pro-inflammatory chemokine homologues that promote neutrophil recruitment to sites of tissue damage. Targeting neutrophils has mixed effects in animal models of stroke. Neutrophil blockade has so far failed to show therapeutic benefit at clinical trial. [12]
MCP-1 Acute Chemokine for monocytes, hematogenous macrophages, neutrophils, memory T-lymphocytes and natural killer cells. Increases infarct size in animal models of stroke. However, MCP-1/CCR2 signaling has also been shown to reduce hemorrhagic transformation in animal models of stroke. [21, 46]
MIP-1α Acute Chemokine for macrophages, monocytes and neutrophils. Ligand for CCR5. CCR5 deficient mice have increased brain damage after ischemic stroke. However, mice lacking CCR5 in the periphery have reduced brain damage after ischemic stroke. The role of MIP-1α in mediating these mixed results is unknown. [44]
MIP-1β Acute Chemokine for macrophages, monocytes and neutrophils. Also a ligand for CCR5. The role of MIP-1β in mediating the mixed results of targeting CCR5 signaling following stroke is unknown. [11, 44]
RANTES Acute Chemokine for multiple leukocyte subsets, including T cells. Also a ligand for CCR5. Evidence from animal models suggests that RANTES is a primary mediator of cerebral inflammation, blood-brain barrier dysfunction, and tissue damage following stroke [48]
TNFα Acute Pleiotropic pro-inflammatory cytokine that can activate NF-kB signaling, MAPK signaling, and induction of apoptosis in target cells. Both injurious and beneficial roles of TNFα have been demonstrated. Blockade of TNFα reduces infarct volume in animal models of stroke, however pretreating mice with TNFα can be neuroprotective. [2, 34]
IL-6 Liquefactive Necrosis Pro-inflammatory cytokine secreted by T cells and macrophages. An acute increase in IL-6 in the CNS is neuroprotective. A prolonged increase is detrimental. Role in chronic stroke infarcts unknown. [14]
MCP-1 Liquefactive Necrosis Chemokine for monocytes, hematogenous macrophages, neutrophils, memory T-lymphocytes and natural killer cells. Role in chronic stroke infarcts unknown. However, prolonged MCP-1 elevation correlates with poor infarct resolution after spinal cord injury. [18]
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