Alternative activation in systemic juvenile idiopathic arthritis monocytes

Copyright © 2011 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 142(2012), 3 vom: 05. März, Seite 362-72
1. Verfasser: Macaubas, Claudia (VerfasserIn)
Weitere Verfasser: Nguyen, Khoa D, Peck, Ariana, Buckingham, Julia, Deshpande, Chetan, Wong, Elizabeth, Alexander, Heather C, Chang, Sheng-Yung, Begovich, Ann, Sun, Yue, Park, Jane L, Pan, Kuang-Hung, Lin, Richard, Lih, Chih-Jian, Augustine, Erin M, Phillips, Carolyn, Hadjinicolaou, Andreas V, Lee, Tzielan, Mellins, Elizabeth D
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2012
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Cytokines FCGR3B protein, human GPI-Linked Proteins Lipopolysaccharide Receptors Receptors, IgG
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245 1 0 |a Alternative activation in systemic juvenile idiopathic arthritis monocytes 
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520 |a Systemic juvenile idiopathic arthritis (SJIA) is a chronic autoinflammatory condition. The association with macrophage activation syndrome, and the therapeutic efficacy of inhibiting monocyte-derived cytokines, has implicated these cells in SJIA pathogenesis. To characterize the activation state (classical/M1 vs. alternative/M2) of SJIA monocytes, we immunophenotyped monocytes using several approaches. Monocyte transcripts were analyzed by microarray and quantitative PCR. Surface proteins were measured at the single cell level using flow cytometry. Cytokine production was evaluated by intracellular staining and ELISA. CD14(++)CD16(-) and CD14(+)CD16(+) monocyte subsets are activated in SJIA. A mixed M1/M2 activation phenotype is apparent at the single cell level, especially during flare. Consistent with an M2 phenotype, SJIA monocytes produce IL-1β after LPS exposure, but do not secrete it. Despite the inflammatory nature of active SJIA, circulating monocytes demonstrate significant anti-inflammatory features. The persistence of some of these phenotypes during clinically inactive disease argues that this state reflects compensated inflammation 
650 4 |a Journal Article 
650 4 |a Research Support, N.I.H., Extramural 
650 4 |a Research Support, Non-U.S. Gov't 
650 7 |a Cytokines  |2 NLM 
650 7 |a FCGR3B protein, human  |2 NLM 
650 7 |a GPI-Linked Proteins  |2 NLM 
650 7 |a Lipopolysaccharide Receptors  |2 NLM 
650 7 |a Receptors, IgG  |2 NLM 
700 1 |a Nguyen, Khoa D  |e verfasserin  |4 aut 
700 1 |a Peck, Ariana  |e verfasserin  |4 aut 
700 1 |a Buckingham, Julia  |e verfasserin  |4 aut 
700 1 |a Deshpande, Chetan  |e verfasserin  |4 aut 
700 1 |a Wong, Elizabeth  |e verfasserin  |4 aut 
700 1 |a Alexander, Heather C  |e verfasserin  |4 aut 
700 1 |a Chang, Sheng-Yung  |e verfasserin  |4 aut 
700 1 |a Begovich, Ann  |e verfasserin  |4 aut 
700 1 |a Sun, Yue  |e verfasserin  |4 aut 
700 1 |a Park, Jane L  |e verfasserin  |4 aut 
700 1 |a Pan, Kuang-Hung  |e verfasserin  |4 aut 
700 1 |a Lin, Richard  |e verfasserin  |4 aut 
700 1 |a Lih, Chih-Jian  |e verfasserin  |4 aut 
700 1 |a Augustine, Erin M  |e verfasserin  |4 aut 
700 1 |a Phillips, Carolyn  |e verfasserin  |4 aut 
700 1 |a Hadjinicolaou, Andreas V  |e verfasserin  |4 aut 
700 1 |a Lee, Tzielan  |e verfasserin  |4 aut 
700 1 |a Mellins, Elizabeth D  |e verfasserin  |4 aut 
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