Regulation of chlamydial spreading from the small intestine to the large intestine by IL-22-producing CD4 T cells.

Following an oral inoculation, descends to the mouse large intestine for long-lasting colonization. However, a mutant that lacks the plasmid-encoded protein pGP3 due to an engineered premature stop codon (designated as CMpGP3S) failed to do so even following an intrajejunal inoculation. This was because a CD4 T cell-dependent immunity prevented the spread of CMpGP3S from the small intestine to the large intestine.

Induction of Transmucosal Protection by Oral Vaccination with an Attenuated Chlamydia.

Chlamydia muridarum has been used to study chlamydial pathogenesis because it induces mice to develop hydrosalpinx, a pathology observed in C. trachomatis-infected women. We identified a C.

Induction of transmucosal protection by oral vaccination with an attenuated .

has been used to study chlamydial pathogenesis since it induces mice to develop hydrosalpinx, a pathology observed in -infected women. We identified a mutant that is no longer able to induce hydrosalpinx. In the current study, we evaluated the mutant as an attenuated vaccine.

Regulation of chlamydial colonization by IFNγ delivered via distinct cells.

The mouse-adapted pathogen Chlamydia muridarum (CM) induces pathology in the mouse genital tract but fails to do so in the gastrointestinal tract. CM is cleared from both the genital tract and small intestine by IFNγ delivered by antigen-specific CD4 T cells but persists for a long period in the large intestine. The long-lasting colonization of CM in the large intestine is regulated by IFNγ delivered by group 3 innate lymphoid cells (ILC3s).