Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 204, Issue 6, Pages 1349-1358Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20061587
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Funding
- NCI NIH HHS [P30 CA068485, CA68485] Funding Source: Medline
- NIAID NIH HHS [R01 AI050080, AI50080] Funding Source: Medline
- NIDDK NIH HHS [P30 DK020593, DK20593] Funding Source: Medline
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We defined the function of type I interferons (IFNs) in defense against reovirus strain type 1 Lang (T1L), which is a double-stranded RNA virus that infects Peyer's patches (PPs) after peroral inoculation of mice. T1L induced expression of mRNA for IFN-alpha, IFN-beta, and Mx-1 in PPs and caused localized intestinal infection that was cleared in 10 d. In contrast, T1L produced fatal systemic infection in IFN alpha R1 knockout (KO) mice with extensive cell loss in lymphoid tissues and necrosis of the intestinal mucosa. Studies of bone-marrow chimeric mice indicated an essential role for hematopoietic cells in IFN-dependent viral clearance. Dendritic cells (DCs), including conventional DCs (cDCs), were the major source of type I IFNs in PPs of reovirus-infected mice, whereas all cell types expressed the antiviral protein Mx-1. Neither NK cells nor signaling via Toll-like receptor 3 or MyD88 were essential for viral clearance. These data demonstrate a requirement for type I IFNs in the control of an intestinal viral infection and indicate that cDCs are a significant source of type I IFN production in vivo. Therefore, innate immunity in PPs is an essential component of host defense that limits systemic spread of pathogens that infect the intestinal mucosa.
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