| Literature DB >> 11357874 |
Abstract
T cell migration into tumor masses is critical to the process of immunologically induced tumor regression. Like other lymphoid populations, T cells are recruited to inflammatory sites depending on the interaction of T cell integrin receptors with their ligands expressed on vasculature. It is increasingly becoming evident that the adhesive capacity of integrins is upregulated by signals from chemokine receptors. A model of intratumoral T cell migration has been established using IL-12 to induce tumor regression. Focusing on this particular model, we review how IL-12 works to upregulate the expression and/or function of chemokines/chemokine receptors as well as adhesion molecules and to induce collaboration between chemokine and adhesion systems. This article will also describe why such an IL-12-induced activation of chemokine and adhesion systems leads to T cell-mediated tumor regression in some tumor models, but not in others.Entities:
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Year: 2001 PMID: 11357874 DOI: 10.1016/s1567-5769(00)00049-7
Source DB: PubMed Journal: Int Immunopharmacol ISSN: 1567-5769 Impact factor: 4.932