Abstract
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). Interestingly, the ILC3-delivered IFNγ can inhibit the human pathogen Chlamydia trachomatis (CT) in the mouse endometrium. Thus, IFNγ produced/delivered by different cells may selectively restrict chlamydial colonization in different tissues. Revealing the underlying mechanisms of chlamydial interactions with IFNγ produced by different cells may yield new insights into both chlamydial pathogenicity and mucosal immunity.