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Updated: May 20, 2026
Assay of Adhesion Under Shear Stress for the Study of T Lymphocyte-Adhesion Molecule Interactions
Published on: June 29, 2016
Inflammatory mimetic microfluidic chip by immobilization of cell adhesion molecules for T cell adhesion
Sung Kyu Kim1, Won Kang Moon, Joo Young Park
1Department of Biotechnology, Yonsei University, 50 Yonsei-ro, Seodaemun-gu, Seoul, Korea.
Insights
A new microfluidic chip models leukocyte-endothelial cell interactions, essential for immune responses and diseases. This tool aids in screening immunosuppressive drugs and functions as a biosensor for diagnostics and drug discovery.
Area of Science:
- Biomedical Engineering
- Cell Biology
- Immunology
Background:
- Leukocyte adhesion to endothelial cells is critical for immune function, inflammation, and cancer metastasis.
- Existing in vitro models using endothelial cell lines have limitations in replicating complex disease conditions.
- Cell adhesion molecules like E-selectin, ICAM-1, and VCAM-1 on endothelial cells mediate these interactions.
Purpose of the Study:
- To develop a novel microfluidic chip that mimics inflammatory conditions and leukocyte-endothelial cell binding.
- To investigate the role of specific adhesion molecules in T cell adhesion.
- To evaluate the chip's utility in drug screening and as a biosensor.
Main Methods:
- Development of an "inflammatory mimetic microfluidic chip" controlling adhesion molecule types and ratios.
- Utilizing Jurkat T cells to study binding dynamics.
- Testing immunosuppressive drugs (tacrolimus, cyclosporine A) to inhibit T cell interactions.
Main Results:
- E-selectin was identified as essential for synergistic Jurkat T cell binding.
- The microfluidic chip successfully emulated physiological T cell migration under specific adhesion molecule ratios.
- Immunosuppressive drugs demonstrated inhibitory effects on T cell adhesion within the chip.
Conclusions:
- The inflammatory mimetic microfluidic chip is a promising tool for T cell adhesion assays and immunosuppressive drug screening.
- The chip's dynamic monitoring capabilities support its use as a biosensor for clinical diagnostics and high-throughput drug screening.
Abstract:
Leukocyte adhesion to adhesion molecules on endothelial cells is important in immune function, cancer metastasis and inflammation. This cell-cell binding is mediated via cell adhesion molecules such as E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) found on endothelial cells. Because these adhesion molecules on endothelial cells vary significantly across several disease conditions such as autoimmune diseases, inflammation or cancer metastasis, investigations of therapeutic agents that down-regulate leukocyte-endothelial interactions have been based on in vitro models using endothelial cell lines. Here we report a new model, an inflammatory mimetic microfluidic chip, which emulates leukocyte binding to cell adhesion molecules (CAM) by controlling the types and ratio of adhesion molecules. In our model, E-selectin was essential for the synergic binding of Jurkat T cells. Immunosuppressive drugs, such as tacrolimus (FK506) and cyclosporine A (CsA), were used to inhibit T cell interactions under the physiologic model of T cell migration at a ratio of 5 : 4.3 : 3.9 (E-selectin : ICAM-1 : VCAM-1). Our results support the potential usefulness of the inflammatory mimetic microfluidic chip as a T cell adhesion assay tool with modified adhesion molecules for applications such as immunosuppressive drug screening. The inflammatory mimetic microfluidic chip can also be used as a biosensor in clinical diagnostics, drug efficacy tests and high throughput drug screening due to the dynamic monitoring capability of the microfluidic chip.
