Figure 6
Figure 6. CTLA-4 antibody blockade precipitates diabetes in young GM-CSF/IL-3–deficient mice. (A) Time course of disease development. GM-CSF/IL-3–deficient (n = 30) or wild-type mice (n = 25) were injected intraperitoneally with 100 μg of anti-CTLA-4 antibody (clone 9H10) three times as indicated (arrows). A cohort of GM-CSF/IL-3–deficient mice (n = 15) was similarly treated with isotype-matched IgG control antibody. (B) Fasting blood sugar levels were determined 50 days after the initiation of antibody injections. Of 30 treated GM-CSF/IL-3–deficient mice, 22 developed fasting hyperglycemia (P < .001 versus all other groups).

CTLA-4 antibody blockade precipitates diabetes in young GM-CSF/IL-3–deficient mice. (A) Time course of disease development. GM-CSF/IL-3–deficient (n = 30) or wild-type mice (n = 25) were injected intraperitoneally with 100 μg of anti-CTLA-4 antibody (clone 9H10) three times as indicated (arrows). A cohort of GM-CSF/IL-3–deficient mice (n = 15) was similarly treated with isotype-matched IgG control antibody. (B) Fasting blood sugar levels were determined 50 days after the initiation of antibody injections. Of 30 treated GM-CSF/IL-3–deficient mice, 22 developed fasting hyperglycemia (P < .001 versus all other groups).

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