Lack of STAT3 signaling in CD4⁺ T cells renders the host susceptible to enteric infection.

A. IL-6 stimulation (20 ng/ml) of splenocytes from CD4stat3-/- mice did not induce the phosphorylation of STAT3 protein, indicating the complete abrogation of the STAT3 signaling in the conditional KO CD4+ T cells. B. Infection kinetics and D. bacterial burden in the feces of mice with conditional deletion of STAT3 in CD4+ T cells (CD4stat3-/-) and littermate controls (STAT3flox/flox) shown as colony forming unit (CFU)/g feces. The dashed line represents the sensitivity of the culture method. **p U test. C. CD4stat3-/- mice exhibited increased susceptibility to colon infection upon inoculation with 5×108 CFU of C. rodentium. Survival is represented by Kaplan-Meier survival curves (n = 4–7 mice/group). *p + T cells are contrasted with littermate mice with a floxed STAT3 gene but without the Cre gene to delete the floxed gene. E. Representative images of gross pathology in the colon of CD4stat3-/- mice and Stat3flox/flox mice infected with C. rodentium for 9 days. The scale bar, 1 cm. F. Representative images of microscopic pathology in the distal colon of CD4stat3-/- mice and STAT3flox/flox controls 9 days after infection with C. rodentium, as assessed by hematoxylin and eosin (H&E) staining (5×). The scale bar, 300 μm. G, H. Crypt hyperplasia scores and crypt length (μm) in the distal colon of CD4stat3-/- mice and STAT3flox/flox controls at 9 days after infection with C. rodentium. Data are the Mean ± SEM from two pooled independent experiments using CD4stat3-/- (n = 10) or STAT3flox/flox (n = 10) mice. *p U test.