Infect Immun. 2012 Jan 30. [Epub ahead of print]
Toxoplasma gondii infection inhibits Th17-mediated spontaneous development of arthritis in IL-1 receptor antagonist-deficient mice.
Washino T, Moroda M, Iwakura Y, Aosai F.
Department of Infection and Host Defense, Chiba University Graduate School of Medicine, 1-8-1 Inohana Chuo-ku, Chiba 260-8670, Japan.
IL-1 receptor antagonist (IL-1Ra)-deficient BALB/c mice develop spontaneous arthritis resembling human rheumatoid arthritis. We herein report that infection with Toxoplasma gondii, an intracellular protozoan, is capable of ameliorating the spontaneous development of arthritis in IL-1Ra-deficient mice. The onset of arthritis development was delayed and the severity score of arthritis was significantly suppressed in T. gondii-infected mice. Expression of IL-12p40 mRNA from CD11c(+) cells of mesenteric lymph nodes (mLN) and spleen markedly increased at 1 week after peroral infection. While CD11c(+) cells also produced IL-10, IL-1β and IL-6, CD4(+) T cells from T. gondii-infected mice expressed significantly high levels of T-bet and IFN- γ mRNA at both mLN and spleen. Levels of GATA-3/IL-4 mRNA or RORγt/IL-17 mRNA decreased in the infected mice, indicating Th1 polarization and the reduction of Th2 and Th17 polarization. The severity of arthritis was related to Th1 polarization accompanied with Th17 reduction, demonstrating the protective role of T. gondii-derived Th1 response against Th17-mediated arthritis in IL-1Ra-deficient mice.
PMID: 22290145 [PubMed - as supplied by publisher]