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The Transmembrane Adaptor Protein LIME Is Essential for Chemokine-Mediated Migration of Effector T Cells to Inflammatiory Sites
- Title
- The Transmembrane Adaptor Protein LIME Is Essential for Chemokine-Mediated Migration of Effector T Cells to Inflammatiory Sites
- Authors
- Park, Inyoung; Son, Myongsun; Ahn, Eunseon; Kim, Young-Woong; Kong, Young-Yun; Yun, Yungdae
- Ewha Authors
- 윤영대; 박인영
- SCOPUS Author ID
- 윤영대; 박인영
- Issue Date
- 2020
- Journal Title
- MOLECULES AND CELLS
- ISSN
- 1016-8478
0219-1032
- Citation
- MOLECULES AND CELLS vol. 43, no. 11, pp. 921 - 934
- Keywords
- chemokine; effector T cells; Lck-interacting transmembrane adaptor 1; migration
- Publisher
- KOREAN SOC MOLECULAR &
CELLULAR BIOLOGY
- Indexed
- SCIE; SCOPUS; KCI
- Document Type
- Article
- Abstract
- Lck-interacting transmembrane adaptor 1 (LIME) has been previously identified as a raft-associated transmembrane protein expressed predominantly in T and B lymphocytes. Although LIME is shown to transduce the immunoreceptor signaling and immunological synapse formation via its tyrosine phosphorylation by Lck, a Src-family kinase, the in vivo function of LIME has remained elusive in the previous studies. Here we report that LIME is preferentially expressed in effector T cells and mediates chemokine-mediated T cell migration. Interestingly, in LIME-/- mice, while T cell receptor stimulation-dependent proliferation, differentiation to effector T cells, cytotoxic T lymphocyte (CTL) function and regulatory T lymphocyte (Treg) function were normal, only T cell-mediated inflammatory response was significantly defective. The reduced inflammation was accompanied by the impaired infiltration of leukocytes and T cells to the inflammatory sites of LIME-/- mice. More specifically, the absence of LIME in effector T cells resulted in the reduced migration and defective morphological polarization in response to inflammatory chemokines such as CCL5 and CXCL10. Consistently, LIME-/- effector T cells were found to be defective in chemokine-mediated activation of Rac1 and Rap1, and dysregulated phosphorylation of Pyk2 and Cas. Taken together, the present findings show that LIME is a critical regulator of inflammatory chemokine-mediated signaling and the subsequent migration of effector T cells to inflammatory sites.
- DOI
- 10.14348/molcells.2020.0124
- Appears in Collections:
- 자연과학대학 > 생명과학전공 > Journal papers
- Files in This Item:
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KSMCB043-11-03 (1).pdf(1.53 MB)
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