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MFG-E8–mediated uptake of apoptotic cells by APCs links the pro- and antiinflammatory activities of GM-CSF
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MFG-E8–mediated uptake of apoptotic cells by APCs links the pro- and antiinflammatory activities of GM-CSF
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Journal Article
MFG-E8–mediated uptake of apoptotic cells by APCs links the pro- and antiinflammatory activities of GM-CSF
2007
Overview
Granulocyte-macrophage colony-stimulating factor (GM-CSF) enhances protection against tumors and infections, but GM-CSF-deficient mice develop inflammatory disease. Here we show that GM-CSF is required for the expression of milk fat globule EGF 8 (MFG-E8) in antigen-presenting cells, and that MFG-E8-mediated uptake of apoptotic cells is a key determinant of GM-CSF-triggered tolerance and immunity. Upon exposure to apoptotic cells, GM-CSF-deficient antigen-presenting cells (APCs) produce an altered cytokine profile that results in decreased Tregs and increased Th1 cells, whereas concurrent ablation of IFN-gamma promotes Th17 cells. In wild-type mice, MFG-E8 attenuates the vaccination activity of GM-CSF-secreting tumor cells through Treg induction, whereas a dominant-negative MFG-E8 mutant potentiates GM-CSF-stimulated tumor destruction through Treg inhibition. These findings clarify the immunoregulatory effects of apoptotic cells and suggest new therapeutic strategies to modulate CD4(+) T cell subsets in cancer and autoimmunity.
Publisher
American Society for Clinical Investigation
Subject
/ Animals
/ Antigen-Presenting Cells - cytology
/ Antigen-Presenting Cells - metabolism
/ Antigens
/ Antigens, Surface - metabolism
/ CD4-Positive T-Lymphocytes - cytology
/ CD4-Positive T-Lymphocytes - immunology
/ CD4-Positive T-Lymphocytes - metabolism
/ Complications and side effects
/ Granulocyte-macrophage colony stimulating factor
/ Granulocyte-Macrophage Colony-Stimulating Factor - deficiency
/ Granulocyte-Macrophage Colony-Stimulating Factor - genetics
/ Granulocyte-Macrophage Colony-Stimulating Factor - metabolism
/ Granulocyte-Macrophage Colony-Stimulating Factor - secretion
/ Kinases
/ Ligands
/ Mice
/ Milk
/ Tumors
