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TRIM32-TAX1BP1-dependent selective autophagic degradation of TRIF negatively regulates TLR3/4-mediated innate immune responses

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TRIM32-deficiency potentiates TLR3/4-mediated immune responses in vivo.

(A) Serum cytokine concentrations in Trim32+/+ and Trim32-/- mice. Sex- and age-matched Trim32+/+ and Trim32-/- mice (n = 6) were injected intraperitoneally with poly(I:C) plus D-galactosamine or LPS for the indicated times and the concentrations of IFN-β, TNFα and IL-6 in the serum were determined by ELISA. (B) Effects of TRIM32-deficiency on poly(I:C) and LPS-induced inflammation in the lungs of mice. Sex- and age-matched Trim32+/+ and Trim32-/- mice were injected intraperitoneally with poly(I:C) (2 μg/g) plus D-galactosamine (1 mg/g) or LPS (10 μg /g) for 6 hours and lung sections were used for histological analysis (H&E staining). (C-D) Effects of TRIM32-deficiency on poly(I:C)- and LPS-induced inflammatory death of mice. Wild-type and Trim32−/− littermates (n = 6) were treated with poly(I:C) plus D-galactosamine (C) or LPS (D) as in (A). The survival rates of the mice were recorded every 4 hours in the following 44 hours. (E) Serum cytokine concentrations in Trim32+/+ and Trim32-/- mice. Sex- and age-matched Trim32+/+ and Trim32-/- mice (n = 5) were injected intraperitoneally with MPLA (3 mg/g) plus D-galactosamine (1 mg/g) for 2 hours and the concentrations of TNFα and IL-6 in the sera were measured by ELISA. (F) Effects of TRIM32-deficiency on MPLA plus D-galactosamine-induced inflammatory death of mice. Sex- and age-matched Trim32+/+ (n = 8) and Trim32-/- mice (n = 6) were injected intraperitoneally with MPLA (3 mg/g) plus D-galactosamine (1 mg/g). The survival rates of the mice were recorded every 4 hours in the following 44 hours. *, p<0.05; **, p<0.01.

Fig 2

doi: https://doi.org/10.1371/journal.ppat.1006600.g002