Dynamics of central and peripheral immunomodulation in a murine glioma model

BMC Immunol. 2009 Feb 18:10:11. doi: 10.1186/1471-2172-10-11.

Abstract

Background: Immunosuppression by gliomas contributes to tumor progression and treatment resistance. It is not known when immunosuppression occurs during tumor development but it likely involves cross-talk among tumor cells, tumor-associated macrophages and microglia (TAMs), and peripheral as well as tumor-infiltrating lymphocytes (TILs).

Results: We have performed a kinetic study of this immunomodulation, assessing the dynamics of immune infiltration and function, within the central nervous system (CNS) and peripherally. PDGF-driven murine glioma cells were injected into the white matter of 13 mice. Four mice were sacrificed 13 days post-injection (dpi), four mice at 26 dpi, and five mice at 40 dpi. Using multiparameter flow cytometry, splenic T cells were assessed for FoxP3 expression to identify regulatory T cells (Tregs) and production of IFN-gamma and IL-10 after stimulation with PMA/ionomycin; within the CNS, CD4+ TILs were quantified, and TAMs were quantified and assessed for TNF-alpha and IL-10 production after stimulation with LPS. Peripheral changes associated with tumor development were noted prior to effects within the CNS. The percentage of FoxP3+ regulatory T cells (Tregs) increased by day 26, with elevated frequencies throughout the duration of the study. This early increase in Tregs was paralleled by an increase in IL-10 production from Tregs. At the final time points examined (tumor morbidity or 40 dpi), there was an increase in the frequency of TAMs with decreased capacity to secrete TNF-alpha. An increase in TIL frequency was also observed at these final time points.

Conclusion: These data provide insight into the kinetics of the immunosuppressive state associated with tumor growth in a murine model of human gliomas. Functional impairment of TAMs occurs relatively late in the course of GBM tumor growth, potentially providing a window of opportunity for therapeutic strategies directed towards preventing their functional impairment.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain Neoplasms / chemically induced
  • Brain Neoplasms / immunology*
  • Brain Neoplasms / pathology
  • CD4 Antigens
  • Cell Movement / immunology
  • Flow Cytometry
  • Forkhead Transcription Factors / genetics
  • Forkhead Transcription Factors / metabolism*
  • Glioma / chemically induced
  • Glioma / immunology*
  • Glioma / pathology
  • Immunosuppression Therapy*
  • Interferon-gamma / metabolism
  • Interleukin-10 / metabolism
  • Lymphocyte Activation
  • Lymphocytes, Tumor-Infiltrating / immunology
  • Macrophages / immunology
  • Macrophages / metabolism
  • Macrophages / pathology
  • Mice
  • Mice, Inbred BALB C
  • Microglia / immunology
  • Microglia / metabolism
  • Microglia / pathology
  • Neoplasms, Experimental / chemically induced
  • Neoplasms, Experimental / immunology*
  • Neoplasms, Experimental / pathology
  • Platelet-Derived Growth Factor / administration & dosage
  • Platelet-Derived Growth Factor / genetics
  • T-Lymphocytes, Regulatory / immunology
  • T-Lymphocytes, Regulatory / metabolism*
  • T-Lymphocytes, Regulatory / pathology
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • CD4 Antigens
  • FOXP3 protein, human
  • Forkhead Transcription Factors
  • Platelet-Derived Growth Factor
  • Tumor Necrosis Factor-alpha
  • Interleukin-10
  • Interferon-gamma