The transition to the metastatic phenotype of rat lymphoma cells involves up-regulation of IL-10 receptor expression and IL-10 secretion.

Interleukin 10 (IL-10) is a Th2 anti-inflammatory cytokine that participates in the regulation of the immune response at several levels. Its production has been implicated in the immunosuppression frequently observed in tumor bearing hosts. The broad spectrum of IL-10 biologic activities is mediated by its binding to its cognate receptor (IL-10R). We have already demonstrated the overproduction of IL-10 by B-cell lymphoma tumor bearing rats and, also, that IL-10 could act as a growth factor for metastatic cells. Considering the importance to unravel each feature of the complex biology of metastasis, the goal of the present study was to investigate the expression of IL-10 receptor (IL-10R), at mRNA and protein level, in primary tumor and metastatic cells from a rat B-cell lymphoma, along with the production of IL-10 by both tumor cell types. Our results indicate that IL-10, besides its immunoregulatory effect, would act as an autocrine growth factor for cells with metastatic phenotype. Also, the up-regulation of IL-10 and IL-10R expression would be part of the transition from primary tumor to the metastatic phenotype.