Suppressed cellular alloimmune responses in HIV-exposed seronegative female sex workers

Jennes, Wim; Evertse, D.; Borget, Marie Yolande; Vuylsteke, Béa; Maurice, Chantal; Nkengasong, John N.; Kestens, Luc

doi:10.1111/j.1365-2249.2006.03017.x

Cited by 43 publications

(32 citation statements)

References 48 publications

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“…For example, commercial sex works that have remained uninfected for at least 7 years, despite high HIV exposure, uniformly show heightened frequencies of Tregs, and a concurrent reduction in the frequencies CD69+-activated T cells. 105 Similar results have been shown in terms of reduction in immune activation for other cohorts of HESN, 102,106,107 potentially implying a contributory role for Tregs in protection from HIV infection. Along these lines, seronegative infants born to HIV-positive mothers, who were not receiving antiretroviral treatment during pregnancy, were found to have enhanced frequencies of Tregs and a reduction in the frequencies of activated effector T cells in cord blood.…”

Section: Chronic Infectionssupporting

confidence: 79%

The Immune Fulcrum

Richert-Spuhler

Lund

2015

Progress in Molecular Biology and Translational Science

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Regulatory T cells (Tregs) are indispensable for immune homeostasis and the prevention of autoimmunity. In the context of infectious diseases, Tregs are multidimensional. Here, we describe how they may potentiate effector responses by assisting in recruitment of T cells into the infection site to resolve infection, facilitate accelerated antigen-specific memory responses, limit pathology, and contribute to disease resolution and healing, to the great benefit of the host. We also explore the villainous functions of Tregs during infection by reviewing several diseases in which the depletion or reduction in Treg frequency allows for better generation of effector memory, and results in acute resolution of infection, as opposed to chronicity or severe long-term outcomes. We describe findings generated using mouse models of infection as well as experiments performed using human cells and tissues. We propose that Tregs represent an immunologic fulcrum, promoting both pathogen clearance and damage control by preventing excessive destruction of infected tissues though unchecked immune responses.

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Section: Chronic Infectionssupporting

confidence: 79%

The Immune Fulcrum

Richert-Spuhler

Lund

2015

Progress in Molecular Biology and Translational Science

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“…Studies of highly exposed MSM showed that HESN individuals had lower levels of CD45RO + memory T cells and a lower percentage of activated CD4 + T cells than HIV-susceptible control subjects 215. Similarly, a study of HESN commercial sex workers from Côte d'Ivoire demonstrated lower expression of the activation marker CD69 in memory subsets of CD4 + and CD8 + T cells after alloimmune stimulation 216.…”

Section: Pathology/symptomatologymentioning

confidence: 97%

Recent Insights into the HIV/AIDS Pandemic

Becerra

Bildstein²,

Gach

2016

MIC

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Etiology, transmission and protection: Transmission of HIV, the causative agent of AIDS, occurs predominantly through bodily fluids. Factors that significantly alter the risk of HIV transmission include male circumcision, condom use, high viral load, and the presence of other sexually transmitted diseases. Pathology/Symptomatology: HIV infects preferentially CD4+ T lymphocytes, and Monocytes. Because of their central role in regulating the immune response, depletion of CD4+ T cells renders the infected individual incapable of adequately responding to microorganisms otherwise inconsequential. Epidemiology, incidence and prevalence: New HIV infections affect predominantly young heterosexual women and homosexual men. While the mortality rates of AIDS related causes have decreased globally in recent years due to the use of highly active antiretroviral therapy (HAART) treatment, a vaccine remains an elusive goal. Treatment and curability: For those afflicted HIV infection remains a serious illness. Nonetheless, the use of advanced therapeutics have transformed a dire scenario into a chronic condition with near average life spans. When to apply those remedies appears to be as important as the remedies themselves. The high rate of HIV replication and the ability to generate variants are central to the viral survival strategy and major barriers to be overcome. Molecular mechanisms of infection: In this review, we assemble new details on the molecular events from the attachment of the virus, to the assembly and release of the viral progeny. Yet, much remains to be learned as understanding of the molecular mechanisms used in viral replication and the measures engaged in the evasion of immune surveillance will be important to develop effective interventions to address the global HIV pandemic.

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“…Recently, an emerging body of literature has also identified a direct association between immune activation and the susceptibility to HIV infection. Studies in macaques [4,5] and humans [6,7,8,9] have reported that an immune quiescent phenotype, manifested by decreased cytokine production, low CD4 + T-cell activation marker expression, suppression of cellular alloimmune responses and decreased CD4 + T-cell gene expression, may confer protection against HIV infection in highly exposed-seronegative individuals. The CAPRISA 004 trial identified that women who became infected with HIV had higher concentrations of proinflammatory cytokines, activated natural killer (NK) cells and CD8 + T-cell degranulation compared with uninfected women, irrespective of tenofovir gel use [10].…”

Section: Introductionmentioning

confidence: 99%

Reduced Immune Activation During Tenofovir–Emtricitabine Therapy in HIV-Negative Individuals

Castillo‐Mancilla

Meditz²,

Wilson

et al. 2015

JAIDS Journal of Acquired Immune Deficiency Syndromes

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Background Elevated immune activation is associated with an increased risk of HIV acquisition. Tenofovir (TFV) has immunomodulatory properties in vitro, but how this extends in vivo remains unknown. Methods HIV-negative adults received daily co-formulated tenofovir-disoproxil-fumarate (TDF) 300 mg/emtricitabine (FTC) 200 mg for 30 days followed by a 30-day washout. Markers of T-cell activation, inflammation and cytokines were measured before drug and on days 30 (on drug) and 60 (30-day washout). Data were analyzed using one-way ANOVA/pairwise comparisons. Intracellular disposition of TFV-diphosphate (TFV-DP) and FTC-triphosphate (FTC-TP) in CD4+ and CD8+ T-cells and monocytes was characterized, and the relationship with immune activation was evaluated using Pearson correlation coefficient. Results T-cell activation was available in 19 participants. CD38/HLA-DR co-expression on CD8+ T-cells decreased from baseline to day 30 (3.97 vs. 2.71%;P=0.03) and day 60 (3.97 vs. 2.41%;P=0.008). Soluble CD27 decreased from baseline to day 60 (184.1 vs. 168.4 pg/ml;P=0.001). Cytokines and inflammation markers were not significantly different. TFV-DP and FTC-TP were approximately 4-fold higher in monocytes vs. CD4+ and CD8+ T-cells, but neither correlated with activation markers. Conclusions TDF/FTC therapy was associated with decreased T-cell activation in HIV-negative adults, which could contribute to the antiviral effect of pre-exposure prophylaxis.

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Suppressed cellular alloimmune responses in HIV-exposed seronegative female sex workers

Cited by 43 publications

References 48 publications

The Immune Fulcrum

The Immune Fulcrum

Recent Insights into the HIV/AIDS Pandemic

Reduced Immune Activation During Tenofovir–Emtricitabine Therapy in HIV-Negative Individuals

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