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suck abstract from ncbi


10.1111/jnc.12135

http://scihub22266oqcxt.onion/10.1111/jnc.12135
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23278273!ä!23278273

suck abstract from ncbi


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pmid23278273      J+Neurochem 2013 ; 125 (1): 74-88
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  • Ly6C+ Ly6G- Myeloid-derived suppressor cells play a critical role in the resolution of acute inflammation and the subsequent tissue repair process after spinal cord injury #MMPMID23278273
  • Saiwai H; Kumamaru H; Ohkawa Y; Kubota K; Kobayakawa K; Yamada H; Yokomizo T; Iwamoto Y; Okada S
  • J Neurochem 2013[Apr]; 125 (1): 74-88 PMID23278273show ga
  • Acute inflammation is a prominent feature of central nervous system (CNS) insult and is detrimental to the CNS tissue. Although this reaction spontaneously diminishes within a short period of time, the mechanism underlying this inflammatory resolution remains largely unknown. In this study, we demonstrated that an initial infiltration of Ly6C(+) Ly6G(-) immature monocyte fraction exhibited the same characteristics as myeloid-derived suppressor cells (MDSCs), and played a critical role in the resolution of acute inflammation and in the subsequent tissue repair by using mice spinal cord injury (SCI) model. Complete depletion of Ly6C(+) Ly6G(-) fraction prior to injury by anti-Gr-1 antibody (clone: RB6-8C5) treatment significantly exacerbated tissue edema, vessel permeability, and hemorrhage, causing impaired neurological outcomes. Functional recovery was barely impaired when infiltration was allowed for the initial 24 h after injury, suggesting that MDSC infiltration at an early phase is critical to improve the neurological outcome. Moreover, intraspinal transplantation of ex vivo-generated MDSCs at sites of SCI significantly reduced inflammation and promoted tissue regeneration, resulting in better functional recovery. Our findings reveal the crucial role of an Ly6C(+) Ly6G(-) fraction as MDSCs in regulating inflammation and tissue repair after SCI, and also suggests an MDSC-based strategy that can be applied to acute inflammatory diseases.
  • |Animals[MESH]
  • |Antibodies/pharmacology[MESH]
  • |Antigens, Ly/*metabolism[MESH]
  • |Female[MESH]
  • |Granulocytes/metabolism/pathology[MESH]
  • |Inflammation/metabolism/pathology[MESH]
  • |Mice[MESH]
  • |Mice, Inbred C57BL[MESH]
  • |Monocytes/metabolism/pathology[MESH]
  • |Myeloid Cells/metabolism/*pathology/transplantation[MESH]
  • |Neovascularization, Physiologic[MESH]
  • |Receptors, Chemokine/immunology[MESH]
  • |Spinal Cord Injuries/*metabolism/pathology/physiopathology[MESH]


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