Alternative Translational Reading Frames as a Novel Source of Epitopes for an Expanded CD8 T-Cell Repertoire: Use of a Retroviral System to Assess the Translational Requirements for CTL Recognition and Lysis

Carlson, Timothy L.; Green, Kathy A.; Green, William R.

doi:10.1089/vim.2010.0057

Cited by 4 publications

(4 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Various other aspects of LP-BM5 infection, and what is known about the cellular and molecular mechanism(s) of LP-BM5 retrovirus induction of pathogenesis (80,81,88,89,95,(102)(103)(104)(105)(106)(107)(108), are interesting to consider in light of a possible role for MDSC function in MAIDS. Our lab and others have documented a critical role for CD4 ϩ T cells in this disease (27,28,68,69,79).…”

Section: Discussionmentioning

confidence: 99%

Myeloid-Derived Suppressor Cells in Murine Retrovirus-Induced AIDS Inhibit T- and B-Cell ResponsesIn VitroThat Are Used To Define the Immunodeficiency

Green

Cook

Green

2013

J Virol

Self Cite

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Myeloid-Derived Suppressor Cells in Murine Retrovirus-Induced AIDS Inhibit T- and B-Cell ResponsesIn VitroThat Are Used To Define the Immunodeficiency

Green

Cook

Green

2013

J Virol

Self Cite

View full text Add to dashboard Cite

“…a slippery sequence and a downstream frameshift stimulatory signal.) Also, it is known that ribosomal frameshifts can contribute to epitopes for an expanded repertoire of cytotoxic CD8 T-cells, but the mechanisms accounting for these frameshifts are not known [29]. The occurrence of programmed translational frameshift events in humans has consequences for the development of novel retroviral drugs.…”

Section: Do Programmed -1 Ribosomal Frameshifts Occur During Translatmentioning

confidence: 99%

Targeting frameshifting in the human immunodeficiency virus

Brakier‐Gingras

Charbonneau

Butcher

2012

Expert Opinion on Therapeutic Targets

View full text Add to dashboard Cite

“…As with AIDS patients, this immunodeficiency leads to an increased incidence of B-cell lineage lymphomas and susceptibility to a variety of opportunistic pathogens [34,38]. In resistant BALB/c mice, we have demonstrated a key protective role of Gag-specific CD8 + cytotoxic T-lymphocytes (CTLs), which are critical for controlling LP-BM5 infection and protecting against retroviral pathogenesis [38-42]. We have not been able to detect such robustly protective CTLs in the susceptible B6 model, strongly suggesting that this CTL deficit is critical to the disease induction.…”

Section: Introductionmentioning

confidence: 99%

The role of indoleamine 2,3-dioxygenase in LP-BM5 murine retroviral disease progression

O’Connor¹,

Green²

2013

Virol J

View full text Add to dashboard Cite

BackgroundIndoleamine 2,3-dioxygenase (IDO) is an immunomodulatory intracellular enzyme involved in tryptophan degradation. IDO is induced during cancer and microbial infections by cytokines, ligation of co-stimulatory molecules and/or activation of pattern recognition receptors, ultimately leading to modulation of the immune response. LP-BM5 murine retroviral infection induces murine AIDS (MAIDS), which is characterized by profound and broad immunosuppression of T- and B-cell responses. Our lab has previously described multiple mechanisms regulating the development of immunodeficiency of LP-BM5-induced disease, including Programmed Death 1 (PD-1), IL-10, and T-regulatory (Treg) cells. Immunosuppressive roles of IDO have been demonstrated in other retroviral models, suggesting a possible role for IDO during LP-BM5-induced retroviral disease progression and/or development of viral load.MethodsMice deficient in IDO (B6.IDO−/−) and wildtype C57BL/6 (B6) mice were infected with LP-BM5 murine retrovirus. MAIDS and LP-BM5 viral load were assessed at termination.ResultsAs expected, IDO was un-inducible in B6.IDO−/− during LP-BM5 infection. B6.IDO−/− mice infected with LP-BM5 retrovirus succumbed to MAIDS as indicated by splenomegaly, serum hyper IgG2a and IgM, decreased responsiveness to B- and T-cell mitogens, conversion of a proportion of CD4+ T cells from Thy1.2+ to Thy1.2-, and increased percentages of CD11b+Gr-1+ cells. LP-BM5 infected B6.IDO−/− mice also demonstrated the development of roughly equivalent disease kinetics as compared to infected B6 mice. Splenic viral loads of B6 and B6.IDO−/− mice were also equivalent after infection as measured by LP-BM5-specific Def Gag and Eco Gag viral mRNA, determined by qRT-PCR.ConclusionsCollectively, these results demonstrate IDO neither plays an essential role, nor is required, in LP-BM5-induced disease progression or LP-BM5 viral load.

show abstract

Alternative Translational Reading Frames as a Novel Source of Epitopes for an Expanded CD8 T-Cell Repertoire: Use of a Retroviral System to Assess the Translational Requirements for CTL Recognition and Lysis

Cited by 4 publications

References 35 publications

Myeloid-Derived Suppressor Cells in Murine Retrovirus-Induced AIDS Inhibit T- and B-Cell ResponsesIn VitroThat Are Used To Define the Immunodeficiency

Myeloid-Derived Suppressor Cells in Murine Retrovirus-Induced AIDS Inhibit T- and B-Cell ResponsesIn VitroThat Are Used To Define the Immunodeficiency

Targeting frameshifting in the human immunodeficiency virus

The role of indoleamine 2,3-dioxygenase in LP-BM5 murine retroviral disease progression

Contact Info

Product

Resources

About