2007年3月
P-selectin glycoprotein ligand-1 mediates L-selectin-independent leukocyte rolling in high endothelial venules of peripheral lymph nodes
INTERNATIONAL IMMUNOLOGY
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- 巻
- 19
- 号
- 3
- 開始ページ
- 321
- 終了ページ
- 329
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1093/intimm/dxl149
- 出版者・発行元
- OXFORD UNIV PRESS
Lymphocyte homing to peripheral lymph nodes (LNs) requires L-selectin. Previous studies, however, suggest that there are L-selectin-independent mechanisms of lymphocyte homing. P-selectin glycoprotein ligand-1 (PSGL-1) is a major ligand for P-selectin expressed in a selectin-binding form on myeloid cells and subsets of lymphoid cells. To discover whether PSGL-1 plays a role in lymphocyte homing, we examined leukocyte rolling and adhesion in the high endothelial venules (HEVs) of the subiliac LNs of wild-type and PSGL-1-deficient mice by intravital microscopy. There were no significant differences in blood velocity or wall shear stress between wild-type and PSGL-1-deficient mice. Although the leukocyte rolling fraction was not altered in PSGL-1-deficient mice, infusion of an anti-L-selectin mAb into these mice completely abolished leukocyte rolling, while the same treatment in wild-type mice inhibited 90% of the leukocyte rolling. This residual rolling in wild-type mice appears to depend on the PSGL-1-P-selectin interaction, since infusion of an anti-L-selectin mAb together with an anti-PSGL-1 mAb or anti-P-selectin mAb almost completely abolished the rolling. PSGL-1 deficiency also led to a higher rolling velocity, suggesting that PSGL-1 mediates leukocyte rolling at low velocities. P-selectin was found to be expressed on the HEVs of subiliac LNs under the conditions of intravital microscopy. Taken together, these results indicate that the interaction of PSGL-1 with P-selectin constitutes a second mechanism of leukocyte rolling in the HEVs of peripheral LNs.
- リンク情報
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- DOI
- https://doi.org/10.1093/intimm/dxl149
- CiNii Articles
- http://ci.nii.ac.jp/naid/10020111395
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/17267415
- Web of Science
- https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000244429500011&DestApp=WOS_CPL
- ID情報
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- DOI : 10.1093/intimm/dxl149
- ISSN : 0953-8178
- CiNii Articles ID : 10020111395
- PubMed ID : 17267415
- Web of Science ID : WOS:000244429500011