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SHIP is required for dendritic cell maturation.

Frann Antignano¹, Mariko Ibaraki, Connie Kim

¹The Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, British Columbia, Canada.

Journal of Immunology (Baltimore, Md. : 1950)

|February 16, 2010

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SHIP negatively regulates dendritic cell (DC) generation but promotes DC maturation and function. SHIP-deficient mice show altered DC development, impacting T cell responses and innate immunity.

Area of Science:

Immunology
Cell Biology
Innate Immunity

Background:

SHIP's role in macrophage development is known, but its function in dendritic cell (DC) generation, maturation, and immune activation is unclear.
Dendritic cells are crucial for initiating adaptive immune responses.

Purpose of the Study:

To investigate the role of SHIP (SH2-containing inositol phosphatase) in the development, maturation, and function of dendritic cells.
To understand SHIP's impact on innate immune activation and T cell responses mediated by DCs.

Main Methods:

Investigated SHIP's role using SHIP-deficient (SHIP(-/-)) mice and bone marrow-derived dendritic cell cultures.
Analyzed DC generation, phenotype, IL-12 secretion upon TLR ligand stimulation, and T cell proliferation.
Utilized PI3K inhibitors (LY294002, wortmannin) to explore the underlying signaling pathways.

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Main Results:

SHIP deficiency led to enhanced DC generation from bone marrow precursors in vitro and increased DC numbers in vivo.
SHIP(-/-) DCs exhibited an immature phenotype and produced significantly lower levels of IL-12 after TLR stimulation.
Reduced IL-12 production in SHIP(-/-) DCs resulted in impaired Ag-specific T cell proliferation and Th1 cell responses.
The immature phenotype of SHIP(-/-) DCs was reversible with PI3K inhibitors, indicating SHIP's regulation of phosphatidylinositol-3,4,5-trisphosphate levels.

Conclusions:

SHIP acts as a negative regulator of GM-CSF-derived dendritic cell generation.
SHIP functions as a positive regulator of dendritic cell maturation and immune function.
SHIP influences dendritic cell development and function by modulating PI3K signaling pathways, impacting adaptive immunity.