Hypothesis: Chlamydia trachomatis infection of the female genital tract is controlled by Type 2 immunity |
| |
| Affiliation: | 1. Instituto Universitario de Biotecnología de Asturias, Departamento de Bioquímica y Biología Molecular, Universidad de Oviedo, 33006 Oviedo, Asturias, Spain;2. Pharmacognosy Research Laboratories, Medway School of Science, University of Greenwich, Central Avenue, Chatham-Maritime, Kent ME4 4TB, UK;3. Servicio de Microbiología, Laboratorio de Virología, Hospital Universitario Central de Asturias, Oviedo, Spain;1. National Heart and Lung Institute, Imperial College London, London SW7 2AZ, UK;1. Department of Medical Parasitology and Infection Biology Swiss Tropical and Public Health Institute, P.O. Box, CH-4002 Basel, Switzerland;2. University of Basel, P.O. Box, CH-4003 Basel, Switzerland;1. Department of Otorhinolaryngology, Head & Neck Surgery, Kansai Medical University, Osaka, Japan;2. Department of Otorhinolaryngology, Takeda General Hospital, Kyoto, Japan;3. Allergy Center, Kansai Medical University, Osaka, Japan;4. Okazaki ENT Clinic, Osaka, Japan;5. Ikeda ENT Clinic, Wakayama, Japan;6. Kawamura ENT Clinic, Osaka, Japan;7. Nakamura ENT Clinic, Osaka, Japan;8. University of Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1011-EGID, Lille, France |
| |
| Abstract: | Chlamydia trachomatis is an obligate intracellular bacterium sexually transmitted to more than 90 million individuals each year. As this level of infectivity implies, C. trachomatis is a successful human parasite; a success facilitated by its ability to cause asymptomatic infection. Host defense against C. trachomatis in the female genital tract is not well defined, but current dogma suggests infection is controlled largely by TH1 immunity. Conversely, it is well established that TH2 immunity controls allergens, helminths, and other extracellular pathogens that cause repetitive or persistent T cell stimulation but do not induce the exuberant inflammation that drives TH1 and TH17 immunity. As C. trachomatis persists in female genital tract epithelial cells but does not elicit over tissue inflammation, we now posit that defense is maintained by Type 2 immune responses that control bacterial growth but minimize immunopathological damage to vital reproductive tract anatomy. Evaluation of this hypothesis may uncover novel mechanisms by which Type 2 immunity can control growth of C. trachomatis and other intracellular pathogens, while confirmation that TH2 immunity was selected by evolution to control C. trachomatis infection in the female genital tract will transform current research, now focused on developing vaccines that elicit strong, and therefore potentially tissue destructive, Chlamydia-specific TH1 immunity. |
| |
| Keywords: | |
| 本文献已被 ScienceDirect 等数据库收录！ |
|
