Figure 4: TNFR-hIg can substantially improve survival rates among nude and Rag-1 knockout mice treated with poly(I:C), and NK cells are critical in the sudden death of Rag-1 knockout mice after poly(I:C) injection. | Nature Medicine

Figure 4: TNFR-hIg can substantially improve survival rates among nude and Rag-1 knockout mice treated with poly(I:C), and NK cells are critical in the sudden death of Rag-1 knockout mice after poly(I:C) injection.

From: Adaptive immune cells temper initial innate responses

Figure 4

(a) T cells inhibited induction of TNF-producing CD11b+ or CD11c+ cells and IFN-γ–producing NK cells in vitro. (b) Decreased inflammatory cytokines from innate cells (CD11b+ cells, NK cells or both) after poly(I:C) in the presence of T cells. (c) Mortality curve of control hIg–treated (, n = 10) and TNFR–hIg–treated nude mice (▪, n = 5) after injection of 700 μg poly(I:C). (d) Mortality curve of Rag-1 knockout mice (hIg: , n = 5 and TNFR-hIg: ▪, n = 5) after poly(I:C) injection. (e) Decreased inflammatory cytokines from non-T cells after poly(I:C) stimulation and addition of soluble TNFR-hIg. (f) Mortality curve of Rag-1 knockout (, n = 8) and NK-depleted Rag-1 knockout (▪, n = 8) mice. (g) Levels of proinflammatory cytokines in serum from Rag-1 knockout and NK-depleted (NK) Rag-1 knockout mice were determined at 2 and 6 h after poly(I:C) injection. *P < 0.05, **P < 0.01, by t-test.

Back to article page