Neonatal Fc receptor for IgG regulates mucosal immune responses to luminal bacteria
J. Clin. Invest. Masaru Yoshida, et al. 116:2142 doi:10.1172/JCI27821 [Go to this article.]

Figure 4
Induction of immune response toC. rodentium –derived antigen in the presence of circulating IgG and FcRn in intestinal epithelial cells. (A and B) The effect of FcRn-mediated IgG transport into the intestinal lumen in C. rodentium infection. Body weight changes (A) and CFU of C. rodentium in feces 21 days after infection (B) in IFABP-mFcRnTg/mβ2mTg/FcRn^–/– and FcRn^–/– C57BL/6 mice with i.v. injection of anti–C. rodentium IgG or control IgG. Mean ± SD are shown for each group (n = 6). (C) Establishment of a genetically engineered C. rodentium strain that constitutively produces an OVA fragment. The immunoblot confirms the expression of the OVA fragment by C. rodentium. (D) Summary of the experimental protocol, with the inoculation of C. rodentium–OVA or control bacteria, the injection of anti–C. rodentium IgG or control IgG, and the adoptive transfer of CD45.1⁺CD4⁺OVA-specific T cells from CD45.1⁺OT-II mice. (E) The number of OVA-specific CD4⁺ T cells in the MLNs in IFABP-mFcRnTg/mβ2mTg/FcRn^–/– and FcRn^–/– mice increased in the presence of anti–C. rodentium IgG or control IgG (n = 3). Arrows indicate increasing rounds of cell division. (F and G) Cytokine production in OVA-specific CD4⁺ T cells purified from the MLNs and cultured with OVA for 48 hours in vitro. Cytokine production of IFN-γ (F) and IL-4 (G) was measured by ELISA. Mean ± SD are shown for each group (n = 4). *P < 0.05.