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-2R alpha beta), the presence of the 0.9 kb transcript specific for the IL-2 gene and, by flow cytometry with anti-IL-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 ELISA. The secreted IL-2 is biologically active since it sustains the proliferation of the IL-2-dependent murine lymphoid 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 fibroblasts 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.
journal_name
Int Immunoljournal_title
International immunologyauthors
Alileche A,Han D,Plaisance S,Assier E,Sahraoui Y,Clemanceau C,Metivier D,Brouty-Boyer D,Jasmin C,Azzarone Bdoi
10.1093/intimm/6.10.1585subject
Has Abstractpub_date
1994-10-01 00:00:00pages
1585-91issue
10eissn
0953-8178issn
1460-2377journal_volume
6pub_type
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