Past Issue

Volume 11, Number 3, Oct-Dec 2017 Pages: 134-141

Recurrent Vulvovaginal Candidiasis: Could It Be Related to Cell-Mediated Immunity Defect in Response to Candida Antigen?

Zahra Talaei, M.D, 1, Saba Sheikhbahaei, M.D, 1, Vajihe Ostadi, Ph.D, 1, Mazdak Ganjalikhani Hakemi, Ph.D, 2, Mohsen Meidani, M.D, 3, Elham Naghshineh, M.D, 4, Majid Yaran, Ph.D, 1, Alireza Emami Naeini, M.D, 1, Roya Sherkat, M.D, 1, *,
Acquired Immunodeficiency Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
Cellular and Molecular Immunology Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
Infectious Diseases and Tropical Medicine Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
Department of Obstetrics Gynecology, Isfahan University of Medical Sciences, Isfahan, Iran
*Corresponding Address: P.O.Box: 81876-98191 Acquired Immunodeficiency Research Center Isfahan University of Medical Sciences Isfahan Iran



Recurrent vulvovaginal candidiasis (RVVC) is a common cause of morbidity affecting millions of women worldwide. Patients with RVVC are thought to have an underlying immunologic defect. This study has been established to evaluate cell-mediated immunity defect in response to candida antigen in RVVC cases.

Materials and Methods

Our cross-sectional study was performed in 3 groups of RVVC patients (cases), healthy individuals (control I) and known cases of chronic mucocutaneous candidiasis (CMC) (control II). Patients who met the inclusion criteria of RVVC were selected consecutively and were allocated in the case group. Peripheral blood mononuclear cells were isolated and labeled with CFSE and proliferation rate was measured in exposure to candida antigen via flow cytometry.


T lymphocyte proliferation in response to candida was significantly lower in RVVC cases (n=24) and CMC patients (n=7) compared to healthy individuals (n=20, P<0.001), but no statistically significant difference was seen between cases and control II group (P>0.05). Family history of primary immunodeficiency diseases (PID) differed significantly among groups (P=0.01), RVVC patients has family history of PID more than control I (29.2 vs. 0%, P=0.008) but not statistically different from CMC patients (29.2 vs. 42.9%, P>0.05). Prevalence of atopy was greater in RVVC cases compared to healthy individuals (41.3 vs. 15%, P=0.054). Lymphoproliferative activity and vaginal symptoms were significantly different among RVVC cases with and without allergy (P=0.01, P=0.02).


Our findings revealed that T cells do not actively proliferate in response to Candida antigen in some RVVC cases. So it is concluded that patients with cell-mediated immunity defect are more susceptible to recurrent fungal infections of vulva and vagina. Nonetheless, some other cases of RVVC showed normal function of T cells. Further evaluations showed that these patients suffer from atopy. It is hypothesized that higher frequency of VVC in patients with history of atopy might be due to allergic response in mucocutaneous membranes rather than a functional impairment in immune system components.