| Literature DB >> 26250807 |
Jaime F Modiano1,2,3,4, Beth A Lindborg5,6,7, Ron T McElmurry8,9, Mitzi Lewellen10,8, Colleen L Forster11, Edward A Zamora12, Jerome Schaack13,14, Donald Bellgrau14,15, Timothy D O'Brien8,5,6, Jakub Tolar8,5,9.
Abstract
The potential of mesenchymal stromal cells (MSCs) to inhibit anti-tumor immunity is becoming increasingly well recognized, but the precise steps affected by these cells during the development of an anti-tumor immune response remain incompletely understood. Here, we examined how MSCs affect the steps required to mount an effective anti-tumor immune response following administration of adenovirus Fas ligand (Ad-FasL) in the Lewis lung carcinoma (LL3) model. Administration of bone marrow-derived MSCs with LL3 cells accelerated tumor growth significantly. MSCs inhibited the inflammation induced by Ad-FasL in the primary tumors, precluding their rejection; MSCs also reduced the consequent expansion of tumor-specific T cells in the treated hosts. When immune T cells were transferred to adoptive recipients, MSCs impaired, but did not completely abrogate the ability of these T cells to promote elimination of secondary tumors. This impairment was associated with a modest reduction in tumor-infiltrating T cells, with a significant reduction in tumor-infiltrating macrophages, and with a reorganization of the stromal environment. Our data indicate that MSCs in the tumor environment reduce the efficacy of immunotherapy by creating a functional and anatomic barrier that impairs inflammation, T cell priming and expansion, and T cell function-including recruitment of effector cells.Entities:
Keywords: Animal model; Cancer; FasL; Mesenchymal stromal cells; Tumor immunotherapy
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Year: 2015 PMID: 26250807 PMCID: PMC4618101 DOI: 10.1007/s00262-015-1749-6
Source DB: PubMed Journal: Cancer Immunol Immunother ISSN: 0340-7004 Impact factor: 6.968