1. Failure to induce oral tolerance to a soluble protein in patients with inflammatory bowel disease 
Thomas A. Kraus, Lisa Toy, Lisa Chan, Joseph Childs, Lloyd Mayer 
Gastroenterology 
Volume 126, Issue 7, Pages (June 2004)
DOI: /j.gastro

2. Figure 1
Normal laboratory volunteers were given (A) no oral KLH, (B) 5 mg KLH, (C) 50 mg KLH, or (D) 250 mg KLH orally on days 0–5 and 10–15, followed by 2 SC immunizations of KLH (100 μg) on days 26 and 35 (A, days 0 and 10). Heparinized venous blood and serum were obtained on days 0 (baseline), 26 (postoral and preimmunization with SC KLH), 35 (postimmunization), and 42 (postbooster). (A) Blood was drawn on days 0, 10, and 17. T-cell proliferation in response to KLH was measured as described in the Materials and Methods section. The response fold increase in 3H thymidine incorporation represents the cpm of the KLH-stimulated cultures divided by the cpm of unstimulated cultures (range of cpm in the unstimulated cultures was 100–1000). Tolerance was defined as an SI < 3 after booster immunization (dashed line).
Gastroenterology  , DOI: ( /j.gastro )

3. Figure 2
Sera were obtained from volunteers either (A) not fed KLH (0 mg), (B) fed KLH 50 mg, or (C) 250 mg per the oral tolerance protocol and immunized with KLH 100 μg SC on days 26 and 35 (days 0 and 10 for nonfed controls). Anti-KLH antibody was determined by ELISA using KLH 10 μg/mL as a capture Ag and developed with a goat anti-human Ig-alkaline phosphatase-conjugated antibody (IgG and IgM). The results are depicted as optical density (OD) units because no specific anti-KLH control antibody is available. All sera were assayed on the same day to control for variability. All sera were stored frozen (−20°C) until the time of assay. Similar data were obtained by using KLH 100 μg as the capture Ag.
Gastroenterology  , DOI: ( /j.gastro )

4. Figure 3
(A) Six UC patients were given no oral KLH, (B) 5 patients were given 5 mg KLH, and (C) 8 patients were given 50 mg KLH orally on days 0–5 and 10–15, followed by 2 SC immunizations of KLH (100 μg) on days 26 and 35 (A, days 0 and 10). Blood was drawn and KLH-specific T-cell proliferation was determined as described in Figure 1. Tolerance was defined as an SI < 3 after booster immunization (dashed line).
Gastroenterology  , DOI: ( /j.gastro )

5. Figure 4
(A) Seven CD patients were given no oral KLH, (B) 4 patients were given 5 mg KLH, and (C) 8 patients were given 50 mg KLH orally on days 0–5 and 10–15, followed by 2 SC immunizations of KLH (100 μg) on days 26 and 35 (A, days 0 and 10). Blood was drawn and KLH-specific T-cell proliferation was determined as described in Figure 1. Tolerance was defined as an SI < 3 after booster immunization (dashed line).
Gastroenterology  , DOI: ( /j.gastro )

6. Figure 5
Sera were obtained from 5-mg KLH-fed normal controls, UC patients, and CD patients. Anti-KLH antibody was determined by ELISA (as described in Figure 2) on day 26 (postoral feeding and preimmunization with KLH). All sera were assayed on the same day to control for variability. All sera were stored frozen (−20°C) until the time of assay. The data are depicted as OD because there is no available anti-KLH control antibody.
Gastroenterology  , DOI: ( /j.gastro )