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TGF-beta1 on osteoimmunology and the bone component cells

DOI: 10.1186/2045-3701-3-4

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Abstract:

Bone is a rigid organ that constitutes part of the endoskeleton of vertebrates. It serves multiple functions; providing mechanical support for joints and tendons, protecting soft tissue or various organs from mechanical stress or trauma, storing minerals, generating hematopoietic cells, and producing hormones. These many functions are regulated by several soluble factors. Interestingly, accumulated evidence indicates that transforming growth factor beta 1 (TGF-β1) plays a critical role in bone formation, mineral storage, and hematopoietic cell generation. In addition, recent progress in the study of the cross-talk between the skeletal system and the immune system (termed osteoimmunology) has revealed shared components and mechanisms between the two systems [1]. This review highlights recent findings focusing on the role of TGF-β1 in bone metabolism and osteoimmunology.TGF-β1 is a one of the most potent regulatory cytokines with diverse effects on hematopoietic cells. In the immune system, TGF-β1 induces and maintains immune tolerance by regulation of lymphocyte proliferation, differentiation, and survival. Disruption of TGF-β1 results in a dysregulated immune system [2], leading to inappropriate immune cell activation, inflammation, cancer (Leukemia and malignant lymphoma etc) and autoimmune diseases [3]. In fact, TGF-β1-deficient mice (TGF-β1ko) die within 2-3 weeks after birth due to lymphocyte and monocyte infiltration of multiple vital organs [3,4]. CD4+Foxp3+ T cells that predominantly produce anti-inflammatory cytokines (TGF-β, IL-10), but not inflammatory cytokines (IFN-γ, TNF-α, and IL-17) are known as regulatory T cells (Tregs). They inhibit the action of other effector T cells through soluble factors (TGF-β or IL-10) or cell-to-cell contact [5]. It is well known that TGF-β suppresses inflammatory cytokine production by effector T cells, and additionally, it drives the differentiation of na?ve T cells to CD4+CD25+Foxp3+ Tregs [6]. Moreover, TGF-β controls t

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