Immunotherapy for persistent viral infections and associated disease

Burg, Sjoerd H. van der; Arens, Ramon; Melief, Cornelis J.M.

doi:10.1016/j.it.2010.12.006

Cited by 45 publications

(29 citation statements)

References 74 publications

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“…This is in agreement with a study in human where transient CD70 costimulation of Tregs inhibited their suppressive function and converted them into Th1 cells (39). Tregs can respond to therapeutic vaccination, as has been observed upon vaccination with long peptides in human patients (41). However, we did not observe any effect of exogenous helper epitope inclusion on Treg expansion after vaccination.…”

Section: Discussionsupporting

confidence: 93%

CD27 Agonism Plus PD-1 Blockade Recapitulates CD4+ T-cell Help in Therapeutic Anticancer Vaccination

et al. 2016

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Section: Discussionsupporting

confidence: 93%

CD27 Agonism Plus PD-1 Blockade Recapitulates CD4+ T-cell Help in Therapeutic Anticancer Vaccination

et al. 2016

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“…The local concentration of IFN-c-producing HBV-specific CD8 1 T cells in liver has been demonstrated as being key to the func- tional restoration of anti-HBV-specific immunity in persistent HBV infection. 54,55 IFN-c also promotes a non-cytopathic mechanism of HBV elimination that can limit liver damage during the immune-clearance of HBV. 56 Consistent with this, we observed infiltration of IFN-c-producing CD8 1 T cells in the livers of HBsAg-Tg mice in the 33GM-CSF1rHBVvac treated group (Figure 6).…”

Section: Discussionmentioning

confidence: 99%

Overcoming HBV immune tolerance to eliminate HBsAg-positive hepatocytes via pre-administration of GM-CSF as a novel adjuvant for a hepatitis B vaccine in HBV transgenic mice

Wang

Dong²,

Xiao

et al. 2015

Cell Mol Immunol

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Granulocyte-macrophage colony-stimulating factor (GM-CSF) is known to be a potential vaccine adjuvant despite contradictory results from animal and human studies. The discrepancies may be due to the different doses and regimens of GM-CSF that were used, given that either mature or immature dendritic cells (DCs) could be induced under different conditions. To test the hypothesis that GM-CSF can be used as a novel adjuvant for a hepatitis B virus (HBV) therapeutic vaccine, we administered GM-CSF once per day for three days prior to vaccination with recombinant HBV vaccine (rHBVvac) in mice. We observed greater DC maturation in these pre-treated animals at day 3 as compared to day 1 or day 2 of daily GM-CSF administration. This strategy was further investigated for its ability to break the immune tolerance established in hepatitis B surface antigen-transgenic (HBsAg-Tg) animals. We found that the levels of induced anti-HBsAg antibodies were significantly higher in animals following three days of GM-CSF pre-treatment before rHBV vaccination after the third immunization. In addition to the increase in anti-HBsAg antibody levels, cell-mediated anti-HBsAg responses, including delayed-type hypersensitivity, T-cell proliferation, interferon-c production, and cytotoxic T lymphocytes, were dramatically enhanced in the three-day GM-CSF pre-treated group. After adoptive transfers of CD8 1 T cells from immunized animals, antigen-specific CD8 1 T cells were observed in the livers of recipient HBsAg-Tg animals. Moreover, the three-day pre-treatments with GM-CSF prior to rHBVvac vaccination could significantly eliminate HBsAg-positive hepatocytes, suggesting beneficial therapeutic effects. Therefore, this protocol utilizing GM-CSF as an adjuvant in combination with the rHBVvac vaccine has the potential to become a novel immunotherapy for chronic hepatitis B patients. Cellular & Molecular Immunology

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“…It is well known that these viruses can reactivate when immunity is suppressed, suggesting that constant immune surveillance is required to prevent their reactivation (49, 50). They induce responses of virus-specific CD8+ T cells which can be detected long after the virus is controlled (51). Among these viruses HIV, inducing a distinct and well characterized viral disease at any age, was shown to be constantly replicating and causing an antigen-dependent clonal expansion of the memory T cells somewhat resembling what is found in the aging immune system (52).…”

Section: What Might Then Cause These Changes In Adaptive Immunity Witmentioning

confidence: 99%

Human T Cell Aging and the Impact of Persistent Viral Infections

Fülöp¹,

Larbi²,

Pawelec³

2013

Front. Immunol.

300

201

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Aging is associated with a dysregulation of the immune response, loosely termed “immunosenescence.” Each part of the immune system is influenced to some extent by the aging process. However, adaptive immunity seems more extensively affected and among all participating cells it is the T cells that are most altered. There is a large body of experimental work devoted to the investigation of age-associated differences in T cell phenotypes and functions in young and old individuals, but few longitudinal studies in humans actually delineating changes at the level of the individual. In most studies, the number and proportion of late-differentiated T cells, especially CD8+ T cells, is reported to be higher in the elderly than in the young. Limited longitudinal studies suggest that accumulation of these cells is a dynamic process and does indeed represent an age-associated change. Accumulations of such late-stage cells may contribute to the enhanced systemic pro-inflammatory milieu commonly seen in older people. We do not know exactly what causes these observed changes, but an understanding of the possible causes is now beginning to emerge. A favored hypothesis is that these events are at least partly due to the effects of the maintenance of essential immune surveillance against persistent viral infections, notably Cytomegalovirus (CMV), which may exhaust the immune system over time. It is still a matter of debate as to whether these changes are compensatory and beneficial or pathological and detrimental to the proper functioning of the immune system and whether they impact longevity. Here, we will review present knowledge of T cell changes with aging and their relation to chronic viral and possibly other persistent infections.

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Immunotherapy for persistent viral infections and associated disease

Cited by 45 publications

References 74 publications

CD27 Agonism Plus PD-1 Blockade Recapitulates CD4+ T-cell Help in Therapeutic Anticancer Vaccination

CD27 Agonism Plus PD-1 Blockade Recapitulates CD4+ T-cell Help in Therapeutic Anticancer Vaccination

Overcoming HBV immune tolerance to eliminate HBsAg-positive hepatocytes via pre-administration of GM-CSF as a novel adjuvant for a hepatitis B vaccine in HBV transgenic mice

Human T Cell Aging and the Impact of Persistent Viral Infections

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