AI Article Synopsis
- A microfluidics-based skin-on-chip model is created to study T lymphocyte migration in skin inflammation and test new drugs.
- Findings show that a modified CCL20 can inhibit T cell movement, indicating potential for psoriasis treatment.
- The model also reveals that the S1P background reduces T cell egress and that inflammatory cytokines can stimulate T cell movement, allowing detailed, quantitative analysis of these processes.
Article Abstract
A microfluidics-based three-dimensional skin-on-chip (SoC) model is developed in this study to enable quantitative studies of transendothelial and transepithelial migration of human T lymphocytes in mimicked skin inflammatory microenvironments and to test new drug candidates. The keys results include 1) CCL20-dependent T cell transmigration is significantly inhibited by an engineered CCL20 locked dimer (CCL20LD), supporting the potential immunotherapeutic use of CCL20LD for treating skin diseases such as psoriasis; 2) transepithelial migration of T cells in response to a CXCL12 gradient mimicking T cell egress from the skin is significantly reduced by a sphingosine-1-phosphate (S1P) background, suggesting the role of S1P for T cell retention in inflamed skin tissues; and 3) T cell transmigration is induced by inflammatory cytokine stimulated epithelial cells in the SoC model. Collectively, the developed SoC model recreates a dynamic multi-cellular micro-environment that enables quantitative studies of T cell transmigration at a single cell level in response to physiological cutaneous inflammatory mediators and potential drugs.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8058301 | PMC |
| http://dx.doi.org/10.1039/d0lc01194k | DOI Listing |
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