Crosstalk among IL-23 and DNAX activating protein of 12 kDa-dependent pathways promotes osteoclastogenesis
IL-23 has been well studied in the context of T cell differentiation; however, its role in the differentiation of myeloid progenitors is less clear. In this paper, we describe a novel role of IL-23 in myeloid cell differentiation. Specifically, we have identified that in human PBMCs, IL-23 induces t...
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| Veröffentlicht in: | The Journal of immunology (1950) 2015-01, Vol.194 (1), p.316-324 |
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| container_title | The Journal of immunology (1950) |
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| creator | Shin, Hyun-Seock Sarin, Ritu Dixit, Neha Wu, Jian Gershwin, Eric Bowman, Edward P Adamopoulos, Iannis E |
| description | IL-23 has been well studied in the context of T cell differentiation; however, its role in the differentiation of myeloid progenitors is less clear. In this paper, we describe a novel role of IL-23 in myeloid cell differentiation. Specifically, we have identified that in human PBMCs, IL-23 induces the expression of MDL-1, a PU.1 transcriptional target during myeloid differentiation, which orchestrates osteoclast differentiation through activation of DNAX activating protein of 12 kDa and its ITAMs. The molecular events that lead to the differentiation of human macrophages to terminally differentiated osteoclasts are dependent on spleen tyrosine kinase and phospholipase Cγ2 phosphorylation for the induction of intracellular calcium flux and the subsequent activation of master regulator osteoclast transcription factor NFATc1. IL-23-elicited osteoclastogenesis is independent of the receptor activator of NF-κB ligand pathway and uses a unique myeloid DNAX activating protein of 12 kDa-associated lectin-1(+)/DNAX activating protein of 12 kDa(+) cell subset. Our data define a novel pathway that is used by IL-23 in myeloid cells and identify a major mechanism for the stimulation of osteoclastogenesis in inflammatory arthritis. |
| doi_str_mv | 10.4049/jimmunol.1401013 |
| format | Article |
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In this paper, we describe a novel role of IL-23 in myeloid cell differentiation. Specifically, we have identified that in human PBMCs, IL-23 induces the expression of MDL-1, a PU.1 transcriptional target during myeloid differentiation, which orchestrates osteoclast differentiation through activation of DNAX activating protein of 12 kDa and its ITAMs. The molecular events that lead to the differentiation of human macrophages to terminally differentiated osteoclasts are dependent on spleen tyrosine kinase and phospholipase Cγ2 phosphorylation for the induction of intracellular calcium flux and the subsequent activation of master regulator osteoclast transcription factor NFATc1. IL-23-elicited osteoclastogenesis is independent of the receptor activator of NF-κB ligand pathway and uses a unique myeloid DNAX activating protein of 12 kDa-associated lectin-1(+)/DNAX activating protein of 12 kDa(+) cell subset. 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In this paper, we describe a novel role of IL-23 in myeloid cell differentiation. Specifically, we have identified that in human PBMCs, IL-23 induces the expression of MDL-1, a PU.1 transcriptional target during myeloid differentiation, which orchestrates osteoclast differentiation through activation of DNAX activating protein of 12 kDa and its ITAMs. The molecular events that lead to the differentiation of human macrophages to terminally differentiated osteoclasts are dependent on spleen tyrosine kinase and phospholipase Cγ2 phosphorylation for the induction of intracellular calcium flux and the subsequent activation of master regulator osteoclast transcription factor NFATc1. IL-23-elicited osteoclastogenesis is independent of the receptor activator of NF-κB ligand pathway and uses a unique myeloid DNAX activating protein of 12 kDa-associated lectin-1(+)/DNAX activating protein of 12 kDa(+) cell subset. Our data define a novel pathway that is used by IL-23 in myeloid cells and identify a major mechanism for the stimulation of osteoclastogenesis in inflammatory arthritis.</description><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>Arthritis - immunology</subject><subject>Arthritis - metabolism</subject><subject>Calcium - metabolism</subject><subject>Cell Differentiation</subject><subject>Cells, Cultured</subject><subject>Enzyme Activation</subject><subject>Humans</subject><subject>Interleukin-23 - metabolism</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Lectins, C-Type - biosynthesis</subject><subject>Macrophage Activation - immunology</subject><subject>Macrophages - cytology</subject><subject>Macrophages - immunology</subject><subject>Membrane Proteins - metabolism</subject><subject>Multiprotein Complexes - biosynthesis</subject><subject>Myeloid Progenitor Cells - cytology</subject><subject>NFATC Transcription Factors - biosynthesis</subject><subject>NFATC Transcription Factors - metabolism</subject><subject>Osteoclasts - cytology</subject><subject>Osteoclasts - metabolism</subject><subject>Phospholipase C gamma - metabolism</subject><subject>Phosphorylation</subject><subject>Protein Structure, Quaternary</subject><subject>Protein-Tyrosine Kinases - metabolism</subject><subject>RANK Ligand - metabolism</subject><subject>Receptors, Cell Surface - biosynthesis</subject><subject>Receptors, Interleukin - metabolism</subject><subject>Signal Transduction</subject><subject>Syk Kinase</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkTtPw0AQhE8IREKgp0JX0jjsPW2XUXhFiqABic46n9fBie0Lvgso_x5HSWiptthvRrszhFwzGEuQ6d2yappN6-oxk8CAiRMyZEpBpDXoUzIE4DxisY4H5ML7JQBo4PKcDLiSiisth2Q57Zz3wdQrahrXLuhsHnFBTVvQ-5fJBzU2VN8mVP1m3bmAVUtdSRmnq3sTFbjGtsA20LUJnz9m63dQ02OeOh_Q2dr44BbYoq_8JTkrTe3x6jBH5P3x4W36HM1fn2bTyTyyUkKIMIfUcpUoXoqc9y8ksbVxHItUlLnUeYqK2bRkulDIULKEg2QMFc9TjSIHMSK3e9_-lq8N-pA1lbdY16ZFt_EZSyDRqVJc_I9qkcodGvco7FG7C6zDMlt3VWO6bcYg25WRHcvIDmX0kpuD-yZvsPgTHNMXv5UfhlQ</recordid><startdate>20150101</startdate><enddate>20150101</enddate><creator>Shin, Hyun-Seock</creator><creator>Sarin, Ritu</creator><creator>Dixit, Neha</creator><creator>Wu, Jian</creator><creator>Gershwin, Eric</creator><creator>Bowman, Edward P</creator><creator>Adamopoulos, Iannis E</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7QP</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>20150101</creationdate><title>Crosstalk among IL-23 and DNAX activating protein of 12 kDa-dependent pathways promotes osteoclastogenesis</title><author>Shin, Hyun-Seock ; 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however, its role in the differentiation of myeloid progenitors is less clear. In this paper, we describe a novel role of IL-23 in myeloid cell differentiation. Specifically, we have identified that in human PBMCs, IL-23 induces the expression of MDL-1, a PU.1 transcriptional target during myeloid differentiation, which orchestrates osteoclast differentiation through activation of DNAX activating protein of 12 kDa and its ITAMs. The molecular events that lead to the differentiation of human macrophages to terminally differentiated osteoclasts are dependent on spleen tyrosine kinase and phospholipase Cγ2 phosphorylation for the induction of intracellular calcium flux and the subsequent activation of master regulator osteoclast transcription factor NFATc1. IL-23-elicited osteoclastogenesis is independent of the receptor activator of NF-κB ligand pathway and uses a unique myeloid DNAX activating protein of 12 kDa-associated lectin-1(+)/DNAX activating protein of 12 kDa(+) cell subset. 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| subjects | Adaptor Proteins, Signal Transducing - metabolism Arthritis - immunology Arthritis - metabolism Calcium - metabolism Cell Differentiation Cells, Cultured Enzyme Activation Humans Interleukin-23 - metabolism Intracellular Signaling Peptides and Proteins - metabolism Lectins, C-Type - biosynthesis Macrophage Activation - immunology Macrophages - cytology Macrophages - immunology Membrane Proteins - metabolism Multiprotein Complexes - biosynthesis Myeloid Progenitor Cells - cytology NFATC Transcription Factors - biosynthesis NFATC Transcription Factors - metabolism Osteoclasts - cytology Osteoclasts - metabolism Phospholipase C gamma - metabolism Phosphorylation Protein Structure, Quaternary Protein-Tyrosine Kinases - metabolism RANK Ligand - metabolism Receptors, Cell Surface - biosynthesis Receptors, Interleukin - metabolism Signal Transduction Syk Kinase |
| title | Crosstalk among IL-23 and DNAX activating protein of 12 kDa-dependent pathways promotes osteoclastogenesis |
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