Enhanced Induction of Very Late Antigen 4/Lymphocyte Function-associated Antigen 1-dependent T-Cell Migration to Tumor Sites following Administration of Interleukin 12

摘要: Administration of interleukin 12 (IL-12) into mice bearing CSA1M, OV-HM, Meth A, or MCH-1-A1 tumor induced complete regression CSA1M and OV-HM tumors but only a slight growth inhibition A tumors. These effects IL-12 were associated with high marginal levels T-cell infiltration CSA1M/OV-HM A/MCH-1-A1 masses, respectively. Here, we investigated the role in induction migration. Spleen cells from untreated IL-12-treated CSA1M-bearing stained vitro fluorescein chemical transferred i.v. IL-12-untreated mice. Migration donor was quantitated by counting number fluorescent on cryostat sections masses. Although migration detected for spleen as well normal mice, enhanced observed similar model. In contrast, such an enhancement models. Immunohistochemical studies revealed that predominant subset CD4+ CD8+ Consistent this observation, dominant migrating T found to be inhibited pretreatment recipients either combination anti-very late antigen 4 + anti-vascular cell adhesion molecule 1 anti-lymphocyte function-associated antiintercellular monoclonal antibody. results indicate can confer capacity migrate sites through very 4/lymphocyte pathways vivo acquisition following treatment correlates regression.