Journal:

Article Title: Injury Induces Deficient Interleukin-12 Production, But Interleukin-12 Therapy After Injury Restores Resistance to Infection

doi:

Figure Lengend Snippet: Figure 1. Interleukin-12 p70 secretion by lipopolysaccharide-stimulated adherent cells from the peripheral blood mononuclear cells of 27 burn and trauma patients measured by enzyme-linked immunoadsorbent assay on 53 occasions at serial intervals after injury and compared with 18 normal control subjects. The patients’ adherent cells produced significantly less interleukin-12 than cells from normal persons at multiple intervals beginning early after injury.

Article Snippet: In the human assay, the capture antibody was a mouse antihuman IL-12 p70 monoclonal antibody (MAB611) and the detection antibody was a biotinylated goat antihuman IL-12 monoclonal antibody (BAF219) (both antibodies from R&D Systems, Minneapolis, MN).

Techniques: Produced

Journal:

Article Title: Injury Induces Deficient Interleukin-12 Production, But Interleukin-12 Therapy After Injury Restores Resistance to Infection

doi:

Figure Lengend Snippet: Figure 2. Production of interleukin-12 (IL-12) and IL-10 by lipopolysaccharide-stimulated peripheral blood mononuclear cells (PBMCs) of burn and trauma patients at serial intervals after injury. Thirty-eight observations of IL-10 production were made in 18 patients and 21 observations of IL-12 production in 8 of the same patients. PBMC IL-12 production was significantly diminished in the 8- to 14-day interval after injury when compared with simultaneously studied normal subjects. At the same interval, IL-10 production by the patients’ PBMCs was significantly elevated.

Article Snippet: In the human assay, the capture antibody was a mouse antihuman IL-12 p70 monoclonal antibody (MAB611) and the detection antibody was a biotinylated goat antihuman IL-12 monoclonal antibody (BAF219) (both antibodies from R&D Systems, Minneapolis, MN).

Techniques:

Journal:

Article Title: Injury Induces Deficient Interleukin-12 Production, But Interleukin-12 Therapy After Injury Restores Resistance to Infection

doi:

Figure Lengend Snippet: Figure 3. Survival of groups of 12 to 15 burn and sham burn mice after cecal ligation and puncture performed 10 days after injury. Burn mice receiving 5 ng interleukin-12 (IL-12) every other day for 9 days beginning on the day of injury had a survival similar to that of sham burn mice. IL-12 in a 10-ng dose appeared to have a less favorable effect on survival, and the addition of indomethacin to the 5-ng dose of IL-12 produced inferior results. IL-12 treatment did not affect the survival of sham burn mice.

Article Snippet: In the human assay, the capture antibody was a mouse antihuman IL-12 p70 monoclonal antibody (MAB611) and the detection antibody was a biotinylated goat antihuman IL-12 monoclonal antibody (BAF219) (both antibodies from R&D Systems, Minneapolis, MN).

Techniques: Ligation, Produced

Journal:

Article Title: Injury Induces Deficient Interleukin-12 Production, But Interleukin-12 Therapy After Injury Restores Resistance to Infection

doi:

Figure Lengend Snippet: Figure 4. Survival of groups of 12 to 15 burn and sham burn mice after cecal ligation and puncture performed on day 10 after injury. The burn mice treated with 5 ng interleukin-12 (IL-12) every other day had a survival similar to that of sham burn controls, even though the IL-12 treatment was continued through day 11, beyond the time of cecal ligation and puncture. Untreated burn animals had the expected high death rate.

Article Snippet: In the human assay, the capture antibody was a mouse antihuman IL-12 p70 monoclonal antibody (MAB611) and the detection antibody was a biotinylated goat antihuman IL-12 monoclonal antibody (BAF219) (both antibodies from R&D Systems, Minneapolis, MN).

Techniques: Ligation

Journal:

Article Title: Injury Induces Deficient Interleukin-12 Production, But Interleukin-12 Therapy After Injury Restores Resistance to Infection

doi:

Figure Lengend Snippet: Figure 5. Survival of groups of 12 to 15 burn and sham burn mice after cecal ligation and puncture performed on day 10 after injury. The dose of 1 ng interleukin-12 (IL-12) given every other day in burn animals and continued beyond the time of cecal ligation and puncture produced survival equivalent to that of sham burn controls.

Article Snippet: In the human assay, the capture antibody was a mouse antihuman IL-12 p70 monoclonal antibody (MAB611) and the detection antibody was a biotinylated goat antihuman IL-12 monoclonal antibody (BAF219) (both antibodies from R&D Systems, Minneapolis, MN).

Techniques: Ligation, Produced

Journal:

Article Title: Injury Induces Deficient Interleukin-12 Production, But Interleukin-12 Therapy After Injury Restores Resistance to Infection

doi:

Figure Lengend Snippet: Figure 7. Interferon-gamma production by anti-CD3 antibody-stimulated splenocytes from groups of 5 to 10 burn and sham burn animals 10 days or 13 days after injury (after cecal ligation and puncture on day 10). The burn groups treated with interleukin-12 (IL-12) produced significantly more interferon-gamma than untreated animals. S and S/12 indicate untreated and IL-12–treated sham mice. B and B/12 indicate untreated and IL-12–treated burn mice.

Article Snippet: In the human assay, the capture antibody was a mouse antihuman IL-12 p70 monoclonal antibody (MAB611) and the detection antibody was a biotinylated goat antihuman IL-12 monoclonal antibody (BAF219) (both antibodies from R&D Systems, Minneapolis, MN).

Techniques: Ligation, Produced

Journal:

Article Title: Injury Induces Deficient Interleukin-12 Production, But Interleukin-12 Therapy After Injury Restores Resistance to Infection

doi:

Figure Lengend Snippet: Figure 8. Tumor necrosis factor-alpha production by lipopolysaccharide-stimulated adherent splenocytes from groups of 5 to 10 burn and sham burn animals 10 days or 13 days after injury (after cecal ligation and puncture on day 10). Splenocyte production of tumor necrosis factor-alpha was markedly increased in the burn animals treated with interleukin-12.

Article Snippet: In the human assay, the capture antibody was a mouse antihuman IL-12 p70 monoclonal antibody (MAB611) and the detection antibody was a biotinylated goat antihuman IL-12 monoclonal antibody (BAF219) (both antibodies from R&D Systems, Minneapolis, MN).

Techniques: Ligation

Journal:

Article Title: Injury Induces Deficient Interleukin-12 Production, But Interleukin-12 Therapy After Injury Restores Resistance to Infection

doi:

Figure Lengend Snippet: Figure 9. Production of interleukin-10 (IL-10) by anti-CD3–stimulated splenocytes harvested from groups of 5 to 10 burn and sham burn mice before cecal ligation and puncture on day 10 after injury or on day 13 (after cecal ligation and puncture on day 10). IL-12 treatment increased IL-10 production by burn splenocytes, both before and after cecal ligation and puncture. Splenocytes from untreated burn animals produced more IL-10 than sham burn splenocytes at both intervals.

Article Snippet: In the human assay, the capture antibody was a mouse antihuman IL-12 p70 monoclonal antibody (MAB611) and the detection antibody was a biotinylated goat antihuman IL-12 monoclonal antibody (BAF219) (both antibodies from R&D Systems, Minneapolis, MN).

Techniques: Ligation, Produced

Journal:

Article Title: Injury Induces Deficient Interleukin-12 Production, But Interleukin-12 Therapy After Injury Restores Resistance to Infection

doi:

Figure Lengend Snippet: Figure 10. Total mononuclear cells per spleen in groups of five burn and sham burn animals at day 10 after the burn and at day 13, 3 days after cecal ligation and puncture was performed on day 10. The mononuclear cell population in the spleen was markedly reduced 3 days after cecal ligation and puncture, and treatment with interleukin-12 significantly increased the splenic mononuclear cell population of burn animals.

Article Snippet: In the human assay, the capture antibody was a mouse antihuman IL-12 p70 monoclonal antibody (MAB611) and the detection antibody was a biotinylated goat antihuman IL-12 monoclonal antibody (BAF219) (both antibodies from R&D Systems, Minneapolis, MN).

Techniques: Ligation