L-2 production by myofibroblasts from post-radiation in breast cancer patients

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Abstract
The origin of cell activation in post-radiation fibrosis and its chronic extension are still poorly understood. Since local IL-2 cancer treatment sometimes triggers intraperitoneal fibrosis we have analyzed three myofibroblastic cell strains from post-radiation skin fibrosis (FPR7, FPR10 and FPR15) for their interactions with IL-2. In these cells we have observed the surface expression of the two chains of the IL-2R (IL-2Rαβ), the presence of the 0.9 kb transcript specific for the IL-2 gene and, by flow cytometry with antML-2 mAbs, the presence of IL-2 immunoreactive material inside the cells up to 8 days after subculture. The FPR cell lines secreted IL-2, as determined by EUSA. The secreted IL-2 Is biologically active since it sustains the proliferation of the IL-2-dependent murine lymphold cell line CTLL2 and preincubation with anti-IL-2 blocking mAbs completely abolishes this activity. Overnight incubation of FPR cells with polyclonal anti-IL-2 antibodies leads to a decreased expression of the membrane adhesion molecules ICAM-1 and CD44, suggesting the existence of an autocrine/paracrine loop involved in the surface expression of these antigens. By contrast, in normal adult skin fibroolasts we did not detect IL-2 gene activation. in vivo, IL-2 secretion by post-radiation fibrosis fibroblasts and the subsequent up-regulation of ICAM-1 and CD44 may represent key events during the process that leads to radiation fibrosis.

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