Figure 1. TRIM21 uses anti‐N antibodies to protect against LCMV infection.

• A–F
  Wild‐type (WT) and TRIM21 knockout (KO) mice were infected with 10⁵ FFU LCMV clone 13 (6 mice per group) and 2 mice were uninfected (UI). Weights (A) and Kaplan–Meier survival (B) were compared over 15 days post infection (pi). (C) Sera from WT mice was analysed for N protein (N) and glycoprotein (GP)‐specific antibodies by ELISA, each data point corresponds to one mouse from the same experiment. (D) N‐specific antibody ELISA was used to compare antibody responses in sera of WT and KO mice. (E,F) In vitro neutralisation experiments were performed with sera collected day 8pi from WT, KO and UI mice. (E) Sera was pre‐incubated with LCMV, then the virus‐serum mix was added to MEF cells and LCMV infection titre after 16 h was measured by FFA. (F) Sera was electroporated into MEFs, then cells were plated in triplicate and LCMV was added 4 h later. LCMV infection titre after 16 h was measured by FFA (three replicates).
• G
  Anti‐N mAb KL53 was electroporated into WT and KO MEFs and subsequent LCMV infection titres were measured by FFA.
• H
  Anti‐N mAb KL53 was co‐electroporated with recombinant N protein into WT and KO MEFs, and immunoblotting for N was performed after 3 h. Electroporation of recombinant KL53 expressing the TRIM21 non‐binding mutation H433A was unable to mediate N protein degradation.

Data information: All data are presented as mean with standard error, *P < 0.05, unpaired t‐test.

Source data are available online for this figure.