Receptor activator of nuclear factor-κB ligand in T cells and dendritic cells communication
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The receptor activator of NF-κB ligand (RANKL), a member of the tumor necrosis factor ligand family, has extensive functions beyond osteoclast development. RANKL is expressed in many immune cells such as osteoblasts, osteocytes, marrow stromal cells, activated T cells, synovial cells, keratinocytes, and mammary gland epithelial cells as well as in various tissues. The ligation of RANK by RANKL promotes dendritic cells (DCs) survival through prosurvival signals and the up-regulation of the anti-apoptotic proteins Bcl-2 and Bcl-xL and plays a crucial role in DCs-mediated Th1 differentiation. Therefore, RANKL plays an important role in the regulation of DCs/T cells-mediated specific immunity. This review will briefly inform our current understanding of the role of RANKL signaling in T cells-DCs communication in the immune system.
Abstract
The receptor activator of NF-κB ligand (RANKL), a member of the tumor necrosis factor ligand family, has extensive functions beyond osteoclast development. RANKL is expressed in many immune cells such as osteoblasts, osteocytes, marrow stromal cells, activated T cells, synovial cells, keratinocytes, and mammary gland epithelial cells as well as in various tissues. The ligation of RANK by RANKL promotes dendritic cells (DCs) survival through prosurvival signals and the up-regulation of the anti-apoptotic proteins Bcl-2 and Bcl-xL and plays a crucial role in DCs-mediated Th1 differentiation. Therefore, RANKL plays an important role in the regulation of DCs/T cells-mediated specific immunity. This review will briefly inform our current understanding of the role of RANKL signaling in T cells-DCs communication in the immune system.
참고문헌 (26)
- Akiyama T, "RANKL-RANK interaction in immune regulatory systems", World J ORthop, 3, pp.142~150 (2012)
- Anderson DM, "A homologue of the TNF receptor and its ligand enhance T-cell growth and dendritic-cell function", Nature, 390, pp.175~179 (1997)
- Boyce BF, "Biology of RANK, RANKL, and osteoprotegrin", Arthritis Res Ther, 9, pp.S1~ (2007)
- Burger EH, "Osteoclast formation from mononuclear phagocytes: role of bone -forming cells", J Cell Biol, 99, pp.1901~1906 (1984)
- Caux C, "Activation of human dendritic cells through CD40 cross-linking", J Exp Med, 184, pp.1263~1272 (1994)
- Chan FK, "A domain in TNF receptors that mediates ligand-independent receptor assembly and signaling", Science, 288, pp.2351~2354 (2000)
- Ikedda T, "Determination of three isoforms of the receptor activator of nuclear factor-kB ligand and their differential expression in bone and thymus", Endocrinology, 142, pp.1419~1426 (2001)
- Ito S, "Crytal structure of the extracellular domain of mouse RANK ligand at 2.2Å- resolution", J Biol Chem, 277, pp.6631~6636 (2002)
- Josien R, "TRANCE, a TNF family member, is differentially expressed on T cell subsets and induces cytokine production in dendritic cells", J Immunol, 162, pp.2562~2568 (1999)
- Kartsoginannis V, "Localization of RANKL (receptor activator of NF kappa B ligand) mRNA and protein in skeletal and extraskeleta tissues", Bone, 25, pp.525~534 (1999)
- Kong YY, "Activated T cell regulate bone loss and joint destruction in adjuvant arthritis through osteoprotegerin ligand", Nature, 402, pp.304~313 (1999)
- Lacey DL, "Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation", Cell, 93, pp.165~176 (1998)
- Lam J, "Crystal structure of the TRANCE", RANKL cytokine reveals determinants of receptor-ligand specificity, 2001, pp.108, 971~979
- Leibbrandt A, "RANK", RANKL: Regulators of Immune responses and bone physiology, 2008, pp.1143, 123~150
- Loser K, "Epidermal RANKL controls regulatory T-cell numbers via activation of dendritic cells", Nat Med, 12, pp.1372~1379 (2006)
- Lum L, "Evidence for a role of a tumor necrosis factor-a(TNF-a)-converting Enzyme-like protease in shedding of TRANCE, a TNf family member Involved in osteoclastogenesis and dendritic cell survival", J Biol Chem, 274, pp.13613~13618 (1999)
- Nakashima T, "Protein expression and functional difference of membrane-bound and soluble receptor activator of NF-kB ligand: modulation of the expression by osteotropic factors and cytokines", Biochem Biophys Res Commun, 275, pp.768~775 (2000)
- Rodan GA, "Role of osteoblasts in hormonal control of bone resorption: a hypothesis", Calcif Tissue Int, 33, pp.349~351 (1981)
- Schett G, "Mechanisms of disease: the link between RANKL and arthritic bone disease", Nat Clin Pract Rheumatol, 1, pp.47~54 (2005)
- Tsuda E, "Isolation of a novel cytokine from huma fibrobalsts that specifically inhibits osteoclastogenesis", Biochem Biophys Res Commun, pp.137~142 (1997)
- Wada T, "RANKL-RANK signaling in osteoclastogenesis and bone disease", Trends Mol Med, 12, pp.17~25 (2006)
- Wong BR, "TRANCE is a novel ligand of the tumor necrosis factor receptor family that activates c-Jun N-terminal kinase in T cells", J Biol Chem, 272, pp.25190~25194 (1997)
- Wong BR, "TRANCE (tumor necrosis factor –related activation-induced cytokine), a new TNF family member predominantly expressed in T cells, is a dendritic cell-specific survival factor", J Exp Med, 186, pp.2075~2080 (1997)
- Wong BR, "TRANCE is a novel ligand of the tumor necrosis factor receptor family that activates c-Jun N-terminal KInase in T cells", J Biol Chem, 272, pp.25190~25194 (1997)
- Wong BR, "The TRAF family of signal transducers mediates NF-kappaB activation by the TRANCE receptor", J Biol Chem, 273, pp.28355~28359 (1998)
- Yasuda H, "Osteoclast differentiation factor is a ligand for osteoprotegerin", osteoclastogenesis-inhibitory factor and is identical to TRANCE, Proc Natl Acad Sci USA, pp.1998, 95[DOI]