Cross-presentation: a general mechanism for CTL immunity and tolerance

Carbone, Francis R.; Kurts, Christian; Bennett, Sally R.M.; Miller, J. F. A. P.; Heath, William R.

doi:10.1016/s0167-5699(98)01301-2

Cited by 225 publications

(152 citation statements)

References 62 publications

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“…As the SFV infection is lytic and the infected host cells die by an apoptotic mechanism, 39 it is unclear if the infected cells can act as APC or if the CTL response is generated by uptake of apoptotic bodies into professional APCs, ie by cross-priming. 40 What is clear, however, is that the expressed P815 antigen must be handled very efficiently since doses as low as 100 IU could generate a significant CTL response, as previously also reported for rSFV-NP. 22 100 IU, by definition, can infect a maximum of 100 host cells and, as rSFV is non-replicative, the amount of P815 antigen expressed in these 100 cells must be enough to generate a CTL response.…”

Section: Iu Of Sfv/enh-p1a (Squares) or Sfv-p1a (Black Diamonds) Ormentioning

confidence: 83%

“…injection. The cytotoxic activity was evaluated against P815 cells or against the H-2 d cell line L1210 pulsed with P815A [35][36][37][38][39][40][41][42][43] peptide. As shown in Figure 3a, a strong CTL response was observed when mice were immunized with the SFV constructs carrying P1A.…”

Section: Resultsmentioning

confidence: 99%

“…This supports a cross-priming event, in which material from a few rSFV infected cells could be taken up and processed by a larger number of APCs. 40 Mice immunized with rSFV-P1A failed to develop an antibody response to the P815 antigen, in contrast to the strong anti-NP response to rSFV-NP (data not shown). This could either depend on the subcellular localization of the antigen, as demonstrated in other systems, 41,42 or on a pre-existing self-tolerance against P1A, both at the B and helper T cell levels.…”

Section: Iu Of Sfv/enh-p1a (Squares) or Sfv-p1a (Black Diamonds) Ormentioning

confidence: 92%

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Induction of P815 tumor immunity by recombinant Semliki Forest virus expressing the P1A gene

1999

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The methylcholantrene-induced P815 mastocytoma tumor virus particles (rSFV) were constructed that expressed is derived from DBA/2 mice and expresses a weak tumor variants of the P815 antigen. Such particles, when used rejection antigen, P815A. The P1A gene, which encodes for vaccination, express the antigen only transiently since for the P815A antigen, is silent in most normal tissues with the viral vector is incapable of productive replication. the exception of testis and placenta. These characteristics Nevertheless, mice vaccinated with rSFV generated strong make P815 an interesting mouse model for the human CTL responses and were protected against P815 tumor MAGE-type tumor antigens. Recombinant Semliki Forest challenge.

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Section: Iu Of Sfv/enh-p1a (Squares) or Sfv-p1a (Black Diamonds) Ormentioning

confidence: 83%

Section: Resultsmentioning

confidence: 99%

Section: Iu Of Sfv/enh-p1a (Squares) or Sfv-p1a (Black Diamonds) Ormentioning

confidence: 92%

See 1 more Smart Citation

Induction of P815 tumor immunity by recombinant Semliki Forest virus expressing the P1A gene

1999

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“…The question of whether effective priming of naive CD8 + T cells with specificity for the encoded protein requires the direct transfection of professional antigen presenting cells (APC) by recombinant Ad and thus the expression of endogenous antigens by APC represents a subject of controversial discussion. 32 Crosspriming by APC, ie the MHC class I-restricted presentation of peptides, derived from exogenously uptaken antigens, 33,34 is an alternative mechanism to explain the induction of CD8 + T cells. However, Ad-mediated transfection ex vivo of dendritic cells (DC), which are the critical APC for the initiation of cellular immune responses, has been reported to be an effective method for the generation of protective antitumor T cell immunity.…”

Section: Discussionmentioning

confidence: 99%

Efficacy of recombinant adenovirus as vector for allergen gene therapy in a mouse model of type I allergy

et al. 2002

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DNA-based immunization represents an attractive alternative approach to the current treatment of allergic diseases by specific immunotherapy with allergen extracts. In this study, we used a replication-deficient adenovirus vector (AdCMV), to examine the in vivo efficacy of preventive and therapeutic genetic immunization in a mouse model of type I allergy. Primary immunization with a recombinant adenovirus expressing the model antigen ␤-galactosidase (AdCMV-␤gal) induced a Th1 immune response (predominance of IgG2a antibodies, high frequency of IFN-␥ producing T cells) and large numbers of cytotoxic T lymphocytes. Prophylactic vaccination with AdCMV-␤gal abol-

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“…Several studies have reported a phagosometo-cytosol pathway in APCs to permit MHC Class I presentation of exogenous, particulate proteins (reviewed in Rock, 1996). This cross presentation pathway may represent the major mechanism for priming CTL responses to antigens which are synthesised by other cell types than professional APC (Carbone et al, 1998). Other studies, designed to test the hypothesis that processing and presentation of endogenous antigens through the MHC Class I pathway in DC was more likely to lead to a Th1-type response, showed that infection of the DC with recombinant viruses (adeno-vaccinia or retro-virus) followed by adoptive cell transfer resulted in a potent CTL response that protected mice against lethal tumour challenge (reviewed in Schuler and Steinman, 1997).…”

Section: Impaired Function Of Dendritic Cells In Hcv Infectionmentioning

confidence: 99%

Prospects for dendritic cell vaccination in persistent infection with hepatitis C virus

Gowans

2004

Journal of Clinical Virology

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Although hepatitis C virus (HCV) is classified in the Hepacivirus genus in the family Flaviviridae, it is unlike most of the other members of this family due to its propensity to cause persistent infections. This persistent infection eventually results in chronic liver disease, cirrhosis and hepatocellular carcinoma in a proportion of infected individuals. It has been difficult to examine correlates of clearance or persistence because most acute phase HCV infections are subclinical or result in symptoms which are non-specific; consequently, acute infections are not generally recognised and patients often present many years later with persistent infection and accompanying chronic liver disease. Nevertheless, seminal studies, performed during the acute phase, have identified a number of factors which are likely to influence the outcome of infection, although it is possible that the mechanism is multifactorial. One of these factors is impairment of dendritic cell function by a mechanism resulting from expression of an HCV protein(s) in these cells. This may be a major factor in the failure of the immune response to expand after HCV infection, leading to persistence. Nevertheless, it may be possible to overcome this defect by autologous transfusion of HCV antigen-loaded, mature dendritic cells and the purpose of this review is to highlight the need and general approaches for developing dendritic cell-based immunotherapy for HCV infection.

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Cross-presentation: a general mechanism for CTL immunity and tolerance

Cited by 225 publications

References 62 publications

Induction of P815 tumor immunity by recombinant Semliki Forest virus expressing the P1A gene

Induction of P815 tumor immunity by recombinant Semliki Forest virus expressing the P1A gene

Efficacy of recombinant adenovirus as vector for allergen gene therapy in a mouse model of type I allergy

Prospects for dendritic cell vaccination in persistent infection with hepatitis C virus

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