Microbial translocation augments the function of adoptively transferred self/tumor-specific CD8⁺ T cells via TLR4 signaling
J. Clin. Invest. Chrystal M. Paulos, et al. 117:2197 doi:10.1172/JCI32205 [Go to this article.]

Figure 2
TBI activates the innate immune system and promotes translocation of microorganisms from the radiation-injured gastrointestinal tract. (A and B) TBI induced activation of DCs. Splenocytes and inguinal LNs were isolated from 5 Gy irradiated or nonirradiated mice 1 day after TBI. Absolute numbers of activated CD11c⁺CD86^high DCs in the spleens (A) and inguinal LNs (B) of TBI and nonirradiated C57BL/6 mice were enumerated. Data (n = 3–6 per group) are representative of 3 independent experiments. (C) TBI induced production of inflammatory cytokine IL-12p70. Serum was collected from nonirradiated and 5 Gy TBI mice 1 day after TBI, and IL-12p70 was measured by ELISA. Data (n = 3 per group) are representative of 2 independent experiments. (D) TBI damaged the colon. Colons of mice were analyzed 3 days after TBI and scored by a pathologist blinded to treatment group. Data (n = 3–6 per group) are representative of 2 independent experiments. (E) LPS was elevated in irradiated mice. Serum from nonirradiated and 5 Gy irradiated mice were collected and analyzed for the presence of LPS using a limulus amebocyte lysate assay 6 days after TBI. Data (n = 3–6 per group) are representative of 3 independent experiments. Horizontal bars indicate means. (F) Inflammatory cytokines were elevated in irradiated mice. Serum was collected from nonirradiated and 5 Gy TBI mice 1 day after TBI, and IL-6, IL-1β, and TNF-α cytokines were measured using ELISA. Data are representative of 2 independent experiments. ^††P < 0.05, **P < 0.001 versus nonirradiated mice.