Patterns of Expression of Vaginal T-Cell Activation Markers during Estrogen-Maintained Vaginal Candidiasis

Alsadeq, Ameera; Hamad, Mawieh; Abu-Elteen, Khaled H.

doi:10.1186/1710-1492-4-4-157

Cited by 5 publications

(4 citation statements)

References 24 publications

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“…Furthermore, enhanced expression of CD152 on both vaginal and splenic T cells suggests that estrogen treatment leads to localized as well as systemic suppression of T cell immunity; a key player in the defense against VC. These findings are consistent with previous reports which have shown that estrogen treatment associates with weakened DTH responses [ 14 ], and upregulated expression of T cell inhibitory molecules like CTLA-4 (CD152) [ 29 ]. Estrogen treatment was also shown to induce the expansion of CD4 + CD25 + Treg cells and to enhance their expression of Foxp3 and IL-10 enabling them to suppress naïve T cell proliferation [ 30 ] and hence suppress Th1-mediated protective fungal immunity.…”

Section: Discussionsupporting

confidence: 93%

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Estrogen treatment predisposes to severe and persistent vaginal candidiasis in diabetic mice

Hamad

2014

J Diabetes Metab Disord

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BackgroundIncreased levels of estrogen and diabetes mellitus separately predispose to vaginal candidiasis (VC). However, the compounding effect of estrogen on the severity and persistence of VC in diabetic females is not clear.MethodsTo address this issue, a diabetic mouse model with estrogen-maintained VC was developed and evaluated for vaginal fungal burden (VFB) and immune competence at different time points throughout the study period.ResultsBlood glucose levels in estrogen-treated diabetic mice were consistently lower than that in untreated counterparts. Estrogen-treated C. albicans-infected non-diabetic mice experienced persistent episodes of VC as compared with naïve controls (P < 0.01). However, severity and persistence of VC in estrogen-treated C. albicans-infected diabetic mice was significantly greater than that in non-diabetic counterparts (P < 0.05). Mortality rates among estrogen-treated C. albicans-infected diabetic mice were significantly higher (P < 0.05) than that in non-diabetic counterparts. Statistically significant (P < 0.05) and persistent suppression of the delayed hypersensitivity response (DTH) was evident in estrogen-treated C. albicans-infected diabetic and non-diabetic mice as compared with controls. Levels of expression of the inhibitory molecule CD152 on vaginal and splenic T cells isolated from estrogen-treated C. albicans infected mice was significantly higher than that in naive untreated controls (P < 0.01).ConclusionsThese findings suggest that estrogen treatment in diabetic females may protect against the progression of DM on the one hand and predispose to severe and persistent VC on the other. The later outcome could be related to the immunosuppressed status of the host.

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Section: Discussionsupporting

confidence: 93%

“…10 6 viable cells prepared from vaginal or splenic cell extracts were reacted in 100 μl PBS volumes with FITC-labeled rat anti-mouse CTLA-4 (CD152) (clone 63828) antibody (R&D systems, Emeryville, CA) [ 29 ]. Reaction tubes were kept on ice for 20-25 min before fixation (1 ml of 2% Paraformaldehyde/tube).…”

Section: Methodsmentioning

confidence: 99%

Estrogen treatment predisposes to severe and persistent vaginal candidiasis in diabetic mice

Hamad

2014

J Diabetes Metab Disord

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“…Another molecule that is expressed by mouse T RM in the gut, skin, brain, lung airway, sensory ganglia, and vagina is the transmembrane C‐type lectin CD69 (, authors' unpublished data). CD69 is briefly expressed on all stimulated T cells and is quickly downregulated after activation.…”

Section: Phenotype Of Trmmentioning

confidence: 99%

Tissue‐resident memory T cells

Shin

Iwasaki

2013

Immunological Reviews

178

175

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Summary Tissues such as the genital tract, skin, and lung act as barriers against invading pathogens. To protect the host, incoming microbes must be quickly and efficiently controlled by the immune system at the portal of entry. Memory is a hallmark of the adaptive immune system, which confers long-term protection and is the basis for efficacious vaccines. While the majority of existing vaccines rely on circulating antibody for protection, struggles to develop antibody-based vaccines against infections such as herpes simplex virus (HSV) and human immunodeficiency virus (HIV) have underscored the need to generate memory T cells for robust antiviral control. The circulating memory T-cell population is generally divided into two subsets: effector memory (TEM) and central memory (TCM). These two subsets can be distinguished by their localization, as TCM home to secondary lymphoid organs and TEM circulate through non-lymphoid tissues. More recently, studies have identified a third subset, called tissue-resident memory (TRM) cells, based on its migratory properties. This subset is found in peripheral tissues that require expression of specific chemoattractants and homing receptors for T-cell recruitment and retention, including barrier sites such as the skin and genital tract. In this review, we categorize different tissues in the body based on patterns of memory T-cell migration and tissue residency. This review also describes the rules for TRM generation and the properties that distinguish them from circulating TEM and TCM cells. Finally, based on the failure of recent T-cell-based vaccines to provide optimal protection, we also discuss the potential role of TRM cells in vaccine design against microbes that invade through the peripheral tissues and highlight new vaccination strategies that take advantage of this newly described memory T-cell subset.

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“…Granted that few forms of mycoses (mucocutaneous and dermatophytic infections) occur in healthy and immunocompromised hosts alike, the buck really stops with competent immunity. [9][10][11][12][13] (Table 1). Severe combined immunodeficiency (SCID), selective lymphocyte (e.g.…”

Section: The Buck Stops Herementioning

confidence: 99%

Innate and adaptive antifungal immune responses: partners on an equal footing

Hamad¹

2011

Mycoses

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Adaptive immunity has long been regarded as the major player in protection against most fungal infections. Mounting evidence suggest however, that both innate and adaptive responses intricately collaborate to produce effective antifungal protection. Dendritic cells (DCs) play an important role in initiating and orchestrating antifungal immunity; neutrophils, macrophages and other phagocytes also participate in recognising and eliminating fungal pathogens. Adaptive immunity provides a wide range of effector and regulatory responses against fungal infections. Th1 responses protect against most forms of mycoses but they associate with significant inflammation and limited pathogen persistence. By contrast, Th2 responses enhance persistence of and tolerance to fungal infections thus permitting the generation of long-lasting immunological memory. Although the role of Th17 cytokines in fungal immunity is not fully understood, they can enhance proinflammatory or anti-inflammatory responses or play a regulatory role in fungal immunity all depending on the pathogen, site/phase of infection and host immunostatus. T regulatory cells balance the activities of various Th cell subsets thereby permitting inflammation and protection on the one hand and allowing for tolerance and memory on the other. Here, recent developments in fungal immunity research are reviewed as means of tracing the emergence of a refined paradigm where innate and adaptive responses are viewed in the same light.

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Patterns of Expression of Vaginal T-Cell Activation Markers during Estrogen-Maintained Vaginal Candidiasis

Cited by 5 publications

References 24 publications

Estrogen treatment predisposes to severe and persistent vaginal candidiasis in diabetic mice

Estrogen treatment predisposes to severe and persistent vaginal candidiasis in diabetic mice

Tissue‐resident memory T cells

Innate and adaptive antifungal immune responses: partners on an equal footing

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