The liver is a site for tumor-induced myeloid-derived suppressor cell accumulation and immunosuppression

Dan Ilkovitch, Diana M Lopez

Research output: Contribution to journalArticle

105 Citations (Scopus)

Abstract

Tumor-induced immunosuppression plays a key role in tumor evasion of the immune system. A key cell population recognized as myeloid-derived suppressor cells (MDSC) contributes and helps orchestrate this immunosuppression. MDSC can interact with T cells, macrophages, and natural killer cells to create an environment favorable for tumor progression. In various tumor models, their presence at high levels has been reported in the bone marrow, blood, spleen, and tumor. We report for the first time that MDSC accumulate and home to the liver in addition to the other organs. Liver MDSC suppress T cells and accumulate to levels comparable with splenic MDSC. Additionally, hematopoiesis in the liver contributes to the dramatic expansion of MDSC in this organ. Furthermore, MDSC in the liver interact with macrophages, also known as Kupffer cells, and cause their up-regulation of PD-L1, a negative T-cell costimulatory molecule. The liver is thus an organ in which MDSC accumulate and can contribute to immunosuppression directly and indirectly. MDSC play a role in various pathologic states in addition to cancer, and these results contribute to our understanding of their biology and interactions with immune-related cells.

Original languageEnglish
Pages (from-to)5514-5521
Number of pages8
JournalCancer Research
Volume69
Issue number13
DOIs
StatePublished - Jul 1 2009

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Immunosuppression
Liver
Neoplasms
T-Lymphocytes
Macrophages
Myeloid-Derived Suppressor Cells
Kupffer Cells
Hematopoiesis
Natural Killer Cells
Immune System
Up-Regulation
Spleen
Bone Marrow
Population

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

The liver is a site for tumor-induced myeloid-derived suppressor cell accumulation and immunosuppression. / Ilkovitch, Dan; Lopez, Diana M.

In: Cancer Research, Vol. 69, No. 13, 01.07.2009, p. 5514-5521.

Research output: Contribution to journalArticle

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