التفاصيل البيبلوغرافية
| العنوان: |
Adam17-dependent shedding limits early neutrophil influx but does not alter early monocyte recruitment to inflammatory sites. |
| المؤلفون: |
Jingjing Tang1, Zarbock, Alexander2,3, Gomez, Ivan1, Wilson, Carole L.1, Lefort, Craig T.2, Stadtmann, Anika3, Bell, Bridgit1,4, Li-Chuan Huang1, Klaus Ley2, Raines, Elaine W.1 ewraines@u.washington.edu |
| المصدر: |
Blood. 7/21/2011, Vol. 118 Issue 3, p786-794. 9p. |
| مصطلحات موضوعية: |
*MONOCYTES, *NEUTROPHILS, *PROTEINS, *CELL membranes, *CHIMERISM |
| مستخلص: |
TNF-α-converting enzyme (TACE, herein denoted as Adam17) proteolytically sheds several cell-surface inflammatory proteins, but the physiologic importance of the cleavage of these substrates from leukocyte subsets during inflammation is incompletely understood. In this study, we show that Adam17-null neutrophils have a 2-fold advantage in their initial recruitment during thioglycollate-induced peritonitis, and they roll slower and adhere more readily in the cremaster model than wild-type neutrophils. Although CD44 and ICAM-1 are both in vitro substrates of Adam17, their surface levels are not altered on Adam17-null neutrophils. In contrast, L-selectin levels are elevated up to 10-fold in Adam17-null circulating neutrophils, and their accelerated peritoneal influx, slower rolling, and increased adhesion in the cremaster muscle are dependent on L-selectin. Analysis of mixed chimeras shows that enhanced L-selectin levels and accelerated influx were both cell-intrinsic properties of neutrophils lacking Adam17. In contrast, Adam17-null monocytes display no acceleration of infiltration into the peritoneum in spite of elevated L-selectin surface levels, and their peritoneal influx was independent of L-selectin. Therefore, our data demonstrate substrate and myeloid cell-type specificity of Adam17-mediated cleavage of its substrates, and show that neutrophils and monocytes use distinct mechanisms for infiltration of tissues. [ABSTRACT FROM AUTHOR] |
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