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Collagen type I signaling reduces the expression and the function of human receptor activator of nuclear factor ‐κB ligand (RANKL) in T lymphocytes by Steve Gendron; Julie Couture; Fawzi Aoudjit is a scholarly article available to read on EtoBox.

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## Abstract The mechanisms by which β1 integrins modulate T cell functions are still poorly defined. We have previously reported that signaling __via__ the collagen type I (Coll I) receptor, α2β1 integrin, inhibited FasL expression and protected Jurkat T cells from activation‐induced cell death (AICD). In this study, we examined whether Coll I signaling in T cells also modulates the expression of the human receptor activator of nuclear factor‐κB ligand (RANKL), a recently identified TNF family member which has important functions in osteoclastogenesis, cell survival and apoptosis. Our results show that in both Jurkat T cells and human primary T cells, Coll I signaling significantly reduces activation‐induced RANKL expression by 50–60%. We also found that RANKL is not involved in AICD but participates in doxorubicin‐induced apoptosis of leukemia T cell lines including Jurkat, CEM and HSB‐2. In this respect, Coll I protected leukemia T cell lines from doxorubicin‐induced apoptosis by inhibiting doxorubicin‐induced RANKL expression. Together, our results suggest that by limiting the production of RANKL, Coll I signaling may contribute to the resistance of leukemia T cells to chemother

Author

Steve Gendron; Julie Couture; Fawzi Aoudjit

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Ltd.; Wiley (ISSN 0014-2980)

Published

2005

Language

EN