One requirement for anti-tumor T cells to be effective is their successful traffic to tumor sites. Trafficking of T cells to lymphoid organs and peripheral tissues is a multistage process. Soluble and tissue-bonded chemokines interacting with chemokine receptors expressed by T lymphocytes certainly play a pivotal role in determining migration under physiologic conditions and during inflammation. Therefore a match between the chemokines the tumor produces and the chemokine receptors the effector T cells express is required. Since chemokine produced by the targeted tumor may not match the subset of chemokine receptors expressed by T cells, gene therapy can be used to force the expression of the specific chemokine receptor by effector T cells so that the anti-tumor activity of adoptively transferred anti-tumor T cells is maximized.
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