HIV-specific lymphoproliferative responses in asymptomatic HIV-infected individuals

Pontesilli, O.; Carlesimo, M; Ar, Varani; Ferrara, Rosetta; Ec, Guerra; Ml, Bernardi; Ricci, Giovanni; Am, Mazzone; D’Offizi, Giampiero; Aiuti, F

doi:10.1111/j.1365-2249.1995.tb03716.x

Cited by 27 publications

(3 citation statements)

References 25 publications

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“…Recent evidence implicates Treg in control of HIV-1 and SIV-1 immunity and viral infections (24, 45–53). It is possible that progressive depletion of CD4+ T cells (54, 55) and viral persistence (56–58) seen during AIDS could be ameliorated by Treg depletion from peripheral blood affecting increased anti-HIV CD4+ T cell responses (24, 45, 46, 59). Indeed, Treg maintains suppressive activities for HIV-specific CD4+ and CD8+ T cell responses (30, 50).…”

Section: Discussionmentioning

confidence: 99%

Neuromodulatory Activities of CD4+CD25+ Regulatory T Cells in a Murine Model of HIV-1-Associated Neurodegeneration

Liu

Gong

Huang

et al. 2009

The Journal of Immunology

101

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HIV-1-associated neurocognitive impairments are intrinsically linked to microglial immune activation, persistent viral infection, and inflammation. In the era of antiretroviral therapy, more subtle cognitive impairments occur without adaptive immune compromise. We posit that adaptive immunity is neuroprotective, serving in both the elimination of infected cells through CD8+ cytotoxic T cell activities and the regulation of neuroinflammatory responses of activated microglia. For the latter, little is known. Thus, we studied the neuromodulatory effects of CD4+ regulatory T cells (Treg; CD4+CD25+) or effector T cells in HIV-1-associated neurodegeneration. A newly developed HIV-1 encephalitis mouse model was used wherein murine bone marrow-derived macrophages are infected with a full-length HIV-1YU2/vesicular stomatitis viral pseudotype and injected into basal ganglia of syngeneic immunocompetent mice. Adoptive transfer of CD3-activated Treg attenuated astrogliosis and microglia inflammation with concomitant neuroprotection. Moreover, Treg-mediated anti-inflammatory activities and neuroprotection were associated with up-regulation of brain-derived neurotrophic factor and glial cell-derived neurotrophic factor expression and down-regulation of proinflammatory cytokines, oxidative stress, and viral replication. Effector T cells showed contrary effects. These results, taken together, demonstrate the importance of Treg in disease control and raise the possibility of their utility for therapeutic strategies.

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Section: Discussionmentioning

confidence: 99%

Neuromodulatory Activities of CD4+CD25+ Regulatory T Cells in a Murine Model of HIV-1-Associated Neurodegeneration

Liu

Gong

Huang

et al. 2009

The Journal of Immunology

101

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“…Persistence of HIV is associated with impaired anti-HIV immune responses, as well as many other factors. HIV-specific immune responses become impaired early after infection, even before the loss of responses directed against other antigens (5,6). HIV-specific CD4 + T cell proliferation is undetectable soon after primary infection (7).…”

Section: Introductionmentioning

confidence: 99%

HIV-1 binding to CD4 on CD4+CD25+ regulatory T cells enhances their suppressive function and induces them to home to, and accumulate in, peripheral and mucosal lymphoid tissues: an additional mechanism of immunosuppression

Cloyd

2009

International Immunology

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The establishment and persistence of many chronic infections have been demonstrated to depend on restraint of the vigor of the anti-microbial immune responses by CD4+CD25+ regulatory T (Treg) cells. In HIV-infected individuals, Treg cells suppress both HIV-specific and general CD4+ and CD8+ T cell responses. Increases of CD4+CD25+ Treg cell function during viral infections might be mediated by host-derived pro-inflammatory molecules or directly by viral infection or binding. We examined the effect HIV has upon binding to CD4+CD25+ Treg cells by exposing human purified CD4+CD25+ T cells from healthy donors to HIV-1 in vitro and assessing their Treg-associated functional marker profile and suppressive activities. We found that HIV-1 binding increased their suppressor activities by 2- to 5-fold, which was accompanied by enhanced expression of Treg-associated functional markers sCTLA-4, glucocorticoid-induced tumor necrosis factor receptor and FoxP3. Moreover, HIV-1 binding extended the survival of CD4+CD25+ Treg cells and up-regulated the expression of homing receptors CD62L and integrin alpha4beta7, which in turn would result in Treg cells migrating more rapidly to the peripheral lymph nodes and mucosal lymphoid tissues where anti-HIV immune responses are occurring. Importantly, CD4+CD25+ Treg cells exposed to HIV were not susceptible to homing-induced apoptosis like are other resting CD4+ cells following HIV-1 binding. We show that CD4+CD25+ Treg cells respond directly to HIV-1 itself through HIV gp120 interactions with CD4 molecules. Collectively, our findings explain a mechanism that contributes to the abnormal accumulation of intensified Treg cells in lymphoid and mucosal tissues in HIV patients, resulting in impairment of immune responses which would greatly help HIV persistence.

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“…HIV-specific T-cell proliferative responses are usually poor or absent in HIV-1infected individuals (92)(93)(94). However, strong HIV-specific T-cell proliferative responses associated with production of and antiviral have been found among HIV-1-infected long-term nonprogressors whose viremia was controlled without ARV therapy (95).…”

Section: T-lymphocyte Functionmentioning

confidence: 99%

Monitoring Immune Function

Biberfeld

Lyamuya

AIDS in Africa

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HIV-specific lymphoproliferative responses in asymptomatic HIV-infected individuals

Cited by 27 publications

References 25 publications

Neuromodulatory Activities of CD4+CD25+ Regulatory T Cells in a Murine Model of HIV-1-Associated Neurodegeneration

Neuromodulatory Activities of CD4+CD25+ Regulatory T Cells in a Murine Model of HIV-1-Associated Neurodegeneration

HIV-1 binding to CD4 on CD4+CD25+ regulatory T cells enhances their suppressive function and induces them to home to, and accumulate in, peripheral and mucosal lymphoid tissues: an additional mechanism of immunosuppression

Monitoring Immune Function

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