Journal
NATURE IMMUNOLOGY
Volume 17, Issue 9, Pages 1075-1083Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.3495
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Funding
- NIH NIDDK grant, Pittsburgh Center For Kidney Research, Core B [P30 DK079307]
- Francis Crick Institute, from Medical Research Council
- Cancer Research UK
- Medical Research Council [U117527252]
- Wellcome Trust [089185]
- Biotechnology and Biological Sciences Research Council [BB/L00805X/1]
- US National Institute of Health [DK59530]
- Swiss Multiple Sclerosis Society
- BBSRC [BB/L00805X/1] Funding Source: UKRI
- MRC [MC_U117527252] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/L00805X/1] Funding Source: researchfish
- Medical Research Council [MC_U117527252] Funding Source: researchfish
- The Francis Crick Institute [10194, BB/L502297/1, 10398] Funding Source: researchfish
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Adhesion and migration of T cells are controlled by chemokines and by adhesion molecules, especially integrins, and have critical roles in the normal physiological function of T lymphocytes. Using an RNA-mediated interference screen, we identified the WNK1 kinase as a regulator of both integrin-mediated adhesion and T cell migration. We found that WNK1 is a negative regulator of integrin-mediated adhesion, whereas it acts as a positive regulator of migration via the kinases OXSR1 and STK39 and the ion co-transporter SLC12A2. WNK1-deficient T cells home less efficiently to lymphoid organs and migrate more slowly through them. Our results reveal that a pathway previously known only to regulate salt homeostasis in the kidney functions to balance T cell adhesion and migration.
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