Cellular immunity and Chlamydia genital infection: induction, recruitment, and effector mechanisms

Int Rev Immunol. 2003 Jan-Feb;22(1):3-41. doi: 10.1080/08830180305229.

Abstract

Chlamydia trachomatis is one of the major causes of bacterial sexually transmitted disease worldwide. The initial infection of endocervical epithelium in females is asymptomatic and commonly ascends to fallopian tubes when left untreated. Immunity to Chlamydia develops after infection and appears to provide short-term protection. Consequently, a significant rate of reinfection occurs among sexually active individuals, which can result in reproductive disability. T helper type 1 responses are implicated in providing protective immunity but may also contribute to tubal infertility. The purpose of this chapter is to review the factors that regulate the induction and recruitment of protective cellular immune responses within the local genital mucosa. An understanding of these events is important for the design of a protective vaccine and control of immunopathologic reactions.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Bacterial Vaccines / immunology
  • Chlamydia Infections / epidemiology
  • Chlamydia Infections / immunology*
  • Chlamydia Infections / pathology
  • Chlamydia trachomatis*
  • Cytokines / biosynthesis
  • Female
  • Genital Diseases, Female / epidemiology
  • Genital Diseases, Female / immunology*
  • Genital Diseases, Female / pathology
  • Genitalia, Female / immunology
  • Humans
  • Immunity, Cellular*
  • Immunity, Innate
  • Male
  • Mice
  • T-Lymphocyte Subsets / immunology
  • United States / epidemiology

Substances

  • Bacterial Vaccines
  • Cytokines