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Karl S. Lang, Panco Georgiev, Mike Recher, Alexander A. Navarini, Andreas Bergthaler, Mathias Heikenwalder, Nicola L. Harris, Tobias Junt, Bernhard Odermatt, Pierre-Alain Clavien, Hanspeter Pircher, Shizuo Akira, Hans Hengartner, Rolf M. Zinkernagel
Published in Volume 116, Issue 9
J Clin Invest. 2006; 116(9):2456–2463 doi:10.1172/JCI28349
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Figure 1
TLR3 ligation converts autoreactivity into autoimmune disease.

107 splenocytes from LCMV-gp33/H-2Db–specific TCR-Tg 318 mice were injected i.v. into naive Alb-1 mice or control C57BL/6 mice on day –1. (A) Seven days after transfer, mice were analyzed for gp33-specific T cells and for liver enzymes. Proliferation of transferred cells was analyzed with CFSE (Supplemental Figure 1). (B) After transfer of 318 splenocytes, Alb-1 mice were infected with 200 PFU LCMV-WE on day 0 (filled circles), and numbers of tet-gp33+ CD8+ T cells determined in peripheral blood over time. Serum activities of ALT and bilirubin serum concentrations were also determined (n = 5). *P > 0.05. (C) Mice were immunized with gp33 (1 mg in PBS) and CpG on days 0 and 4 (open squares). A separate group of mice was additionally treated with poly(I:C) on day 7 (arrows) (shaded squares). Numbers of blood tet-gp33+CD8+ T cells, serum ALT activities, and bilirubin serum concentrations were determined (n = 5–7 per group).