Journal
IMMUNITY
Volume 20, Issue 1, Pages 25-35Publisher
CELL PRESS
DOI: 10.1016/S1074-7613(03)00350-9
Keywords
-
Categories
Funding
- NIGMS NIH HHS [GM37734] Funding Source: Medline
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R37GM037734, R01GM037734] Funding Source: NIH RePORTER
Ask authors/readers for more resources
Chemokines regulate rapid leukocyte adhesion by triggering a complex modality of integrin activation. We show that the small GTPase RhoA and the atypical zeta PKC differently control lymphocyte LFA-1 high-affinity state and rapid lateral mobility induced by chemokines. Activation of LFA-1 high-affinity state and lateral mobility is controlled by RhoA through the activity of distinct effector regions, demonstrating that RhoA is a central point of diversification of signaling pathways leading to both modalities of LFA-1 triggering. In contrast, PKC controls LFA-1 lateral mobility but not affinity triggering. Blockade of the 23-40 RhoA effector region prevents induction of LFA-1 high-affinity state as well as lymphocyte arrest in Peyer's patch high endothelial venues. Thus, RhoA controls the induction of LFA-1 high-affinity state by chemokines independently of PKC, and this is critical to support chemokine-regulated homing of circulating lymphocytes.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available