Collagen type I signaling reduces the expression and the function of human receptor activator of nuclear factor -kappaB ligand (RANKL) in T lymphocytes.
The mechanisms by which beta1 integrins modulate T cell functions are still poorly defined. We have previously reported that signaling via the collagen type I (Coll I) receptor, alpha2beta1 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-kappaB 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 chemotherapy. Our study also emphasizes the importance Coll I signaling may have in the control of RANKL-associated T cell functions.[1]References
- Collagen type I signaling reduces the expression and the function of human receptor activator of nuclear factor -kappaB ligand (RANKL) in T lymphocytes. Gendron, S., Couture, J., Aoudjit, F. Eur. J. Immunol. (2005) [Pubmed]
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