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In mouse studies that utilized genetic deletion of interleukin-4 (IL-4), a primary M2-promoting cytokine, the reduction in M2-like macrophages led to fibrotic skin repair with deformed colla- gen fibrils and vascular structures [28], as well as reduced diameters and function of muscle fibers in response to normally regenerative biomate- rials [30].
Koh, Blocking interleukin-1beta induces a
, Implication of interleukin-4 in wound healing, Lab.
, The influence of interleukin-4 on ligament healing, Wound Repair Regen. 19 (3) (2011) 426-435.
, interleukins; iNOS, inducible nitric oxide synthase; LPS, lipopolysaccharide; M-CSF, macrophage colony-stimulating factor; MCP-1/5, monocyte chemoattractant protein-1/5 (CCL2/CCL12); MHCII, major histocompatibility complex class II; MIP- 1α/β, macrophage inflammatory protein-1 alpha/beta (CCL3/CCL4); MNCs, mononuclear cells; MMPs, matrix metalloproteinases; MSCs, mesenchymal stromal cells; NF-κβ, nuclear factor kappa beta; PAMPs, pathogen-associated molecular patterns; PDGF, platelet-derived growth factor; PGE-2, prostaglandin E-2; ROS, reactive oxygen species; TAMs, tumor-associated macrophages; TGF- β1, transforming growth factor beta 1; TNF-α, tumor necrosis factor-alpha; VEGF, vascular endothelial growth factor.
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