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Published on: May 6, 2019
Modulation of CD103 expression on human colon carcinoma-specific CTL
Khoon-Lin Ling1, Nicolas Dulphy, Pru Bahl
1Tumor Immunology Group, Human Immunology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, UK.
Journal of Immunology (Baltimore, Md. : 1950)
|February 22, 2007
Summary
Tumor-infiltrating T cells improve survival in colorectal cancer. This study shows TGF-beta1 and antigen recognition during T cell priming upregulate CD103/beta7, enhancing T cell retention in tumors.
Area of Science:
- Immunology
- Oncology
- Cell Biology
Background:
- Tumor-infiltrating T cells correlate with survival in colorectal cancer.
- Mechanisms of T cell infiltration into colon carcinoma are not fully understood.
- CD103/beta7 integrin expression is known to retain lymphocytes in epithelial layers.
Purpose of the Study:
- To investigate the mechanisms controlling T cell infiltration in human colon carcinoma.
- To determine if CD103/beta7 expression on colon cancer-specific T cells is imprinted during priming.
- To elucidate the role of TGF-beta1 in T cell homing receptor expression.
Main Methods:
- Analysis of CD103/beta7 expression on human colon carcinoma-specific T cells.
- Assessment of synergistic effects of TGF-beta1 and antigen recognition on T cell activation.
- Priming of naive CD8+ T cells with and without TGF-beta1.
Main Results:
- Simultaneous TGF-beta1 stimulation and antigen recognition synergistically enhance CD103/beta7 expression in human colon carcinoma-specific CTLs.
- Priming naive CD8+ T cells with TGF-beta1 upregulates CD103/beta7 for recall responses.
- Lower TGF-beta1 concentrations are required for memory T cells primed with TGF-beta1.
Conclusions:
- TGF-beta1 plays a crucial role during T cell priming in modulating CD103/beta7 expression.
- This modulation controls the retention of human memory CD8+ T cells within the tumor epithelium.
- Understanding these mechanisms may improve T cell-based cancer immunotherapies.
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