Cancer Institute A national cancer institute
designated cancer center

Janice Brown

Publication Details

  • Combined Effects of Interleukin-7 and Stem Cell Factor Administration on Lymphopoiesis after Murine Bone Marrow Transplantation BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION Chung, B., Min, D., Joo, L. W., Krampf, M. R., Huang, J., Yang, Y., Shashidhar, S., Brown, J., Dudl, E. P., Weinberg, K. I. 2011; 17 (1): 48-60

    Abstract:

    The decreased ability of the thymus to generate T cells after bone marrow transplantation (BMT) is a clinically significant problem. Interleukin (IL)-7 and stem cell factor (SCF) induce proliferation, differentiation, and survival of thymocytes. Although previous studies have shown that administration of recombinant human IL-7 (rhIL-7) after murine and human BMT improves thymopoiesis and immune function, whether administration of SCF exerts similar effects is unclear. To evaluate independent or combinatorial effects of IL-7 and SCF in post-BMT thymopoiesis, bone marrow (BM)-derived mesenchymal stem cells transduced ex vivo with the rhIL-7 or murine SCF (mSCF) genes were cotransplanted with T cell-depleted BM cells into lethally irradiated mice. Although rhIL-7 and mSCF each improved immune reconstitution, the combination treatment had a significantly greater effect than either cytokine alone. Moreover, the combination treatment significantly increased donor-derived common lymphoid progenitors (CLPs) in BM, suggesting that transplanted CLPs expand more rapidly in response to IL-7 and SCF and may promote immune reconstitution. Our findings demonstrate that IL-7 and SCF might be therapeutically useful for enhancing de novo T cell development. Furthermore, combination therapy may allow the administration of lower doses of IL-7, thereby decreasing the likelihood of IL-7-mediated expansion of mature T cells.

    View details for DOI 10.1016/j.bbmt.2010.07.027

    View details for Web of Science ID 000286173400003

    View details for PubMedID 20713165

Stanford Medicine Resources:

Footer Links: