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Immunity in vaginal candidiasis.
1Department of Microbiology, Immunology, and Parasitology, Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA. pfidel@lsuhsc.edu
Current Opinion in Infectious Diseases
|March 1, 2005
Summary
Vulvovaginal candidiasis is not caused by T-cell defects. Instead, symptomatic infections involve aggressive polymorphonuclear neutrophil responses, while protection is innate and noninflammatory, challenging previous understandings of Candida immunity.
Area of Science:
- Immunology
- Microbiology
- Women's Health
Background:
- Vulvovaginal candidiasis (VVC) and recurrent VVC are prevalent issues in women of reproductive age.
- Host defense mechanisms against VVC are not well understood.
- Current research challenges established concepts of anti-Candida immunity, particularly the role of T helper 1 (Th1) CD4 T cells.
Purpose of the Study:
- To review recent findings on host defense mechanisms against vulvovaginal candidiasis.
- To investigate the immunological basis of symptomatic versus asymptomatic vulvovaginal candidiasis.
- To re-evaluate the role of T-cell mediated immunity and innate immunity in VVC.
Main Methods:
- Analysis of four recent studies on host defense against VVC.
- Inclusion of data from animal models and human cohorts (adolescents).
- Utilized a natural history protocol involving intravaginal challenge with live Candida.
Main Results:
- Animal models indicated a lack of involvement of systemic or local T-cell-mediated immunity in VVC.
- Antibodies showed a limited role; Candida-specific antibodies were similar or elevated in women with VVC compared to controls.
- Symptomatic VVC correlated with polymorphonuclear neutrophil infiltration, while protection was associated with an innate, noninflammatory response.
Conclusions:
- Symptomatic VVC is linked to an aggressive polymorphonuclear neutrophil response, not defective Th1 CD4 T-cell immunity.
- Protection against VVC appears to be innate and noninflammatory.
- Innate immunity plays a critical, paradigm-shifting role in both protection against and promotion of symptomatic VVC.