J Immunol. 2015 Jun 19. pii: 1500814. [Epub ahead of print]
Sa Q1,
Ochiai E1,
Tiwari A1,
Perkins S1,
Mullins J1,
Gehman M1,
Huckle W2,
Eyestone WH3,
Saunders TL4,
Shelton BJ5,
Suzuki Y6.
Abstract
In vitro studies demonstrated that microglia and astrocytes produce IFN-γ in response to various stimulations, including LPS. However, the physiological role of IFN-γ production by brain-resident cells, including glial cells, in resistance against cerebral infections remains unknown. We analyzed the role of IFN-γ production by brain-resident cells in resistance to reactivation of cerebral infection with Toxoplasma gondii using a murine model. Our study using bone marrow chimeric mice revealed that IFN-γ production by brain-resident cells is essential for upregulating IFN-γ-mediated protective innate immune responses to restrict cerebral T. gondii growth. Studies using a transgenic strain that expresses IFN-γ only in CD11b+ cells suggested that IFN-γ production by microglia, which is the only CD11b+ cell population among brain-resident cells, is able to suppress the parasite growth. Furthermore, IFN-γ produced by brain-resident cells is pivotal for recruiting T cells into the brain to control the infection. These results indicate that IFN-γ produced by brain-resident cells is crucial for facilitating both the protective innate and T cell-mediated immune responses to control cerebral infection with T. gondii.
Copyright © 2015 by The American Association of Immunologists, Inc.
- PMID:
- 26091720
- [PubMed - as supplied by publisher]
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