Induction of NKG2D ligands on human dendritic cells by TLR ligand stimulation and RNA virus infection

@article{citeulike:2705497, abstract = {Monocyte-derived dendritic cells (mDCs) and NK cells are reciprocally activate via cytokines and cellcell contact. Although seven human NKG2D ligands (NKG2DLs), UL16-binding proteins (ULBP) 1, 2, 3 and 4, retinoic acid early transcript 1G (RAET1G) and MHC class I-related chains A and B, have been reported, the differential distribution and roles of these ligands in the maturation of human mDCs have not been elucidated. In the present study, we produced polyclonal antibodies (pAbs) directed against human ULBP1, 2 and 3. All these ULBPs were detected on human mDCs when probed by the pAbs, although their expression profiles were different. We next investigated what kinds of Toll-like receptor agonists and RNA viruses [influenza virus, human respiratory syncytial virus (RSV), measles virus and hepatitis C virus (HCV)] induced the expression of NKG2DLs on mDCs. ULBP1 was up-regulated on mDCs in response to LPS or infection with RSV. The expression of ULBP2 was induced by LPS and poly I:C, indicating that the TIR-containing adapter molecule-1 (TIR domain-containing adaptor-inducing IFN) pathway is associated with ULBP2 induction. Although infection with HCV did not cause up-regulation of NKG2DLs, other RNA virus infections and poly I:C promoted expression of ULBP2 and RAET1G in an IFN-{alpha}/{beta}-independent manner. Finally, the over-expression of ULBP1 and 2 on mDCs facilitated NK cell proliferation and IFN-{gamma} production through a mDCNK cell interaction in the presence of IL-2. Hence, the results reflect the important role of NKG2DLs on human mDCs in mDC-mediated NK cell activation.}, author = {Ebihara, Takashi and Masuda, Hisayo and Akazawa, Takashi and Shingai, Masashi and Kikuta, Hideaki and Ariga, Tadashi and Matsumoto, Misako and Seya, Tsukasa }, citeulike-article-id = {2705497}, doi = {10.1093/intimm/dxm073}, journal = {Int. Immunol.}, keywords = {ra}, month = {October}, pages = {1145--1155}, posted-at = {2008-05-15 01:01:03}, priority = {2}, title = {Induction of NKG2D ligands on human dendritic cells by TLR ligand stimulation and RNA virus infection}, url = {http://intimm.oxfordjournals.org/cgi/content/abstract/19/10/1145}, volume = {19}, year = {2007} }

TY - JOUR ID - citeulike:2705497 L3 - citeulike-article-id:2705497 TI - Induction of NKG2D ligands on human dendritic cells by TLR ligand stimulation and RNA virus infection JF - Int. Immunol. VL - 19 SP - 1145 EP - 1155 N2 - Monocyte-derived dendritic cells (mDCs) and NK cells are reciprocally activate via cytokines and cellcell contact. Although seven human NKG2D ligands (NKG2DLs), UL16-binding proteins (ULBP) 1, 2, 3 and 4, retinoic acid early transcript 1G (RAET1G) and MHC class I-related chains A and B, have been reported, the differential distribution and roles of these ligands in the maturation of human mDCs have not been elucidated. In the present study, we produced polyclonal antibodies (pAbs) directed against human ULBP1, 2 and 3. All these ULBPs were detected on human mDCs when probed by the pAbs, although their expression profiles were different. We next investigated what kinds of Toll-like receptor agonists and RNA viruses [influenza virus, human respiratory syncytial virus (RSV), measles virus and hepatitis C virus (HCV)] induced the expression of NKG2DLs on mDCs. ULBP1 was up-regulated on mDCs in response to LPS or infection with RSV. The expression of ULBP2 was induced by LPS and poly I:C, indicating that the TIR-containing adapter molecule-1 (TIR domain-containing adaptor-inducing IFN) pathway is associated with ULBP2 induction. Although infection with HCV did not cause up-regulation of NKG2DLs, other RNA virus infections and poly I:C promoted expression of ULBP2 and RAET1G in an IFN-{alpha}/{beta}-independent manner. Finally, the over-expression of ULBP1 and 2 on mDCs facilitated NK cell proliferation and IFN-{gamma} production through a mDCNK cell interaction in the presence of IL-2. Hence, the results reflect the important role of NKG2DLs on human mDCs in mDC-mediated NK cell activation. KW - ra AU - Ebihara, Takashi AU - Masuda, Hisayo AU - Akazawa, Takashi AU - Shingai, Masashi AU - Kikuta, Hideaki AU - Ariga, Tadashi AU - Matsumoto, Misako AU - Seya, Tsukasa PY - 2007/October// UR - http://dx.doi.org/10.1093/intimm/dxm073 ER -