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Fluorescence-activated Cell Sorting for Purification of Plasmacytoid Dendritic Cells from the Mouse Bone Marrow
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Published on: November 4, 2016

Functional interaction of plasmacytoid dendritic cells with multiple myeloma cells: a therapeutic target

Dharminder Chauhan1, Ajita V Singh, Mohan Brahmandam

  • 1The LeBow Institute for Myeloma Therapeutics and Jerome Lipper Center for Myeloma Research, Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA. dharminder_chauhan@dfci.harvard.edu

Cancer Cell
|October 6, 2009
PubMed

Insights

Plasmacytoid dendritic cells (pDCs) in the bone marrow microenvironment promote multiple myeloma (MM) growth and drug resistance. Targeting toll-like receptors with CpG oligodeoxynucleotides restores immune function and inhibits MM cell growth, offering a new therapeutic strategy.

Area of Science:

  • Immunology
  • Oncology
  • Hematology

Background:

  • Multiple myeloma (MM) is an incurable plasma cell malignancy.
  • The bone marrow microenvironment plays a critical role in MM pathogenesis and progression.
  • Novel therapeutic strategies are needed to overcome drug resistance in MM.

Purpose of the Study:

  • To investigate the role of plasmacytoid dendritic cells (pDCs) in the bone marrow (BM) microenvironment in MM.
  • To elucidate the mechanisms by which pDCs promote MM cell growth, survival, and drug resistance.
  • To evaluate the therapeutic potential of targeting pDC-MM interactions.

Main Methods:

  • In vitro and in vivo MM xenograft models were utilized.
  • Microarray, cell signaling, cytokine profiling, and immunohistochemical analyses were performed.
  • Toll-like receptor (TLR) agonists (CpG oligodeoxynucleotides) were used to target pDCs.

Main Results:

  • pDCs in the BM microenvironment were found to mediate immune deficiency and promote MM cell growth, survival, and drug resistance.
  • Mechanisms involved complex cell signaling and cytokine profiles.
  • Targeting TLRs with CpG restored pDC immune function and abrogated pDC-induced MM cell growth.

Conclusions:

  • pDCs are key players in the MM bone marrow microenvironment, contributing to immune evasion and therapeutic resistance.
  • Targeting pDC-MM interactions represents a promising therapeutic strategy to overcome drug resistance in multiple myeloma.
  • CpG oligodeoxynucleotides demonstrate potential for restoring immune function and inhibiting MM progression.

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