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Induction of malignant plasma cell proliferation by eosinophils. | LitMetric

AI Article Synopsis

  • The biology of malignant plasma cells in multiple myeloma is significantly influenced by their bone marrow microenvironment, particularly interactions with bone marrow stromal cells, which promote the survival and growth of these cancer cells.
  • This study reveals that eosinophils, a type of immune cell, can enhance the proliferation of malignant plasma cells in the bone marrow by utilizing soluble factors, independent of certain other growth-promoting elements.
  • The research highlights distinct roles for stromal cells and eosinophils in supporting multiple myeloma cell growth and suggests that targeting eosinophils could be a novel therapeutic strategy for treating this disease.

Article Abstract

The biology of the malignant plasma cells (PCs) in multiple myeloma (MM) is highly influenced by the bone marrow (BM) microenvironment in which they reside. More specifically, BM stromal cells (SCs) are known to interact with MM cells to promote MM cell survival and proliferation. By contrast, it is unclear if innate immune cells within this same space also actively participate in the pathology of MM. Our study shows for the first time that eosinophils (Eos) can contribute to the biology of MM by enhancing the proliferation of some malignant PCs. We first demonstrate that PCs and Eos can be found in close proximity in the BM. In culture, Eos were found to augment MM cell proliferation that is predominantly mediated through a soluble factor(s). Fractionation of cell-free supernatants and neutralization studies demonstrated that this activity is independent of Eos-derived microparticles and a proliferation-inducing ligand (APRIL), respectively. Using a multicellular in vitro system designed to resemble the native MM niche, SCs and Eos were shown to have non-redundant roles in their support of MM cell growth. Whereas SCs induce MM cell proliferation predominantly through the secretion of IL-6, Eos stimulate growth of these malignant cells via an IL-6-independent mechanism. Taken together, our study demonstrates for the first time a role for Eos in the pathology of MM and suggests that therapeutic strategies targeting these cells may be beneficial.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3718740PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0070554PLOS

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