Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2018:412:183-215.
doi: 10.1007/82_2016_18.

Immunopathogenesis of Chlamydial Infections

Affiliations
Review

Immunopathogenesis of Chlamydial Infections

Ashlesh K Murthy et al. Curr Top Microbiol Immunol. 2018.

Abstract

Chlamydial infections lead to a number of clinically relevant diseases and induce significant morbidity in human populations. It is generally understood that certain components of the host immune response to infection also mediate such disease pathologies. A clear understanding of pathogenic mechanisms will enable us to devise better preventive and/or intervention strategies to mitigate the morbidity caused by these infections. Over the years, numerous studies have been conducted to explore the immunopathogenic mechanisms of Chlamydia-induced diseases of the eye, reproductive tract, respiratory tract, and cardiovascular systems. In this article, we provide an overview of the diseases caused by Chlamydia, animal models used to study disease pathology, and a historical context to the efforts to understand chlamydial pathogenesis. Furthermore, we discuss recent findings regarding pathogenesis, with an emphasis on the role of the adaptive immune response in the development of chlamydial disease sequelae. Finally, we summarize the key insights obtained from studies of chlamydial pathogenesis and avenues that remain to be explored in order to inform the next steps of vaccine development against chlamydial infections.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Similar articles

Cited by

References

    1. Abbas M, Bobo LD, Hsieh YH, Berka N, Dunston G, Bonney GE, Apprey V, Quinn TC, West SK. Human leukocyte antigen (HLA)-B, DRB1, and DQB1 allotypes associated with disease and protection of trachoma endemic villagers. Invest Ophthalmol Vis Sci. 2009;50:1734–1738. - PMC - PubMed
    1. Adams EJ, Charlett A, Edmunds WJ, Hughes G. Chlamydia trachomatis in the United Kingdom: a systematic review and analysis of prevalence studies. Sex Transm Infect. 2004;80:354–362. - PMC - PubMed
    1. Andrew DW, Cochrane M, Schripsema JH, Ramsey KH, Dando SJ, O’Meara CP, Timms P, Beagley KW. The duration of Chlamydia muridarum genital tract infection and associated chronic pathological changes are reduced in IL-17 knockout mice but protection is not increased further by immunization. PLoS One. 2013;8:e76664. - PMC - PubMed
    1. Arkatkar T, Gupta R, Li W, Yu JJ, Wali S, Neal GM, Chambers JP, Christenson LK, Arulanandam BP. Murine MicroRNA-214 regulates intracellular adhesion molecule (ICAM1) gene expression in genital Chlamydia muridarum infection. Immunology. 2015;145:534–542. - PMC - PubMed
    1. Bai H, Cheng J, Gao X, Joyee AG, Fan Y, Wang S, Jiao L, Yao Z, Yang X. IL-17/Th17 promotes type 1. T cell immunity against pulmonary intracellular bacterial infection through modulating dendritic cell function. J Immunol. 2009;183:5886–5895. - PubMed

LinkOut - more resources