Abstract

RATIONALE: Although Interferon-gamma (IFNγ)-producing CD4 + T-helper (Th)-1 cells are critical to resolve Chlamydia genital tract (GT) infection, these cells, along with neutrophils, have been implicated in development of GT pathology. We examined the neutrophil-inducing CD4 + Th17 response as an alternative mechanism of chlamydial immunopathogenesis.

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