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 IFN gamma 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 IFN gamma delivered by group 3 innate lymphoid cells (ILC3s). Interestingly, the ILC3-delivered IFN gamma can inhibit the human pathogen Chlamydia trachomatis (CT) in the mouse endometrium. Thus, IFN gamma produced/delivered by different cells may selectively restrict chlamydial colonization in different tissues. Revealing the underlying mechanisms of chlamydial interactions with IFN gamma produced by different cells may yield new insights into both chlamydial pathogenicity and mucosal immunity.

Automated summary

The mouse-adapted pathogen Chlamydia muridarum (CM) causes pathology in the mouse genital tract but not in the gastrointestinal tract. Antigen-specific CD4+ T cells that release IFN gamma clear CM from the genital tract and small intestine, while it persists in the large intestine, regulated by IFN gamma delivered by group 3 innate lymphoid cells (ILC3s). Interestingly, ILC3-delivered IFN gamma can inhibit the human pathogen Chlamydia trachomatis (CT) in the mouse endometrium. Understanding the mechanisms of chlamydial interactions with IFN gamma produced by different cells may provide insights into chlamydial pathogenicity and mucosal immunity.