Crawling of effector T cells on extracellular matrix: role of integrins in interstitial migration in inflamed tissues - PubMed (original) (raw)
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Crawling of effector T cells on extracellular matrix: role of integrins in interstitial migration in inflamed tissues
Chang H Kim. Cell Mol Immunol. 2014 Jan.
No abstract available
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Figure 1
Integrins regulate interstitial migration of effector T cells. Circulating memory and effector T cells in the blood circulation enter into tissues through the endothelial cell layer. Adhesion molecules and chemokines cooperatively induce the endothelial cell migration process. Constitutively expressed tissue-specific or inflammation-induced chemokines and adhesion molecules regulate the migration. Integrins play critical roles in transendothelial cell migration by mediating the rolling and firm adhesion process. After transendothelial migration, T cells still need to migrate to specialized microenvironments for their effector functions. This migration is called interstitial migration and involves crawling and squeezing movement on ECM fibers (e.g., collagen and fibronectin), which undergo dramatic alteration to support T-cell migration in inflamed tissues. In inflamed skin, integrins, particularly αV-containing integrins (e.g., αVβ1 and αVβ3), are required for normal interstitial migration of effector T cells. Chemoattractants are likely to be involved in regulating the migration of effector T cells on ECM fibers. Considerable diversity is expected in terms of chemokines and integrins that regulate T-cell migration in different tissues and conditions. ECM, extracellular matrix.
Comment on
- Inflammation-induced interstitial migration of effector CD4⁺ T cells is dependent on integrin αV.
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