Virus and Immune Responses: Lymphocytic Choriomeningitis Virus as a Prototype Model of Viral Pathogenesis

Oldstone, M B; Ahmed, Rafi; Byrne, J. A.; Buchmeier, Michael J.; Rivière, Yves; Southern, Peter J.

doi:10.1093/oxfordjournals.bmb.a072029

Cited by 46 publications

(27 citation statements)

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“…To determine this, we infected Nrf3 Ϫ/Ϫ and control mice with acute LCMV. The CD8, CD4, and B-cell responses to acute LCMV infection have been well characterized (1,51,58). The peak CD8, CD4, and B-cell response to LCMV occurs on day 8 postinfection.…”

Section: Resultsmentioning

confidence: 99%

Complexity of CNC Transcription Factors As Revealed by Gene Targeting of the Nrf3 Locus

Derjuga¹,

Gourley

Holm

et al. 2004

Molecular and Cellular Biology

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Cap'n'collar (CNC) family basic leucine zipper transcription factors play crucial roles in the regulation of mammalian gene expression and development. To determine the in vivo function of the CNC protein Nrf3 (NF-E2-related factor 3), we generated mice deficient in this transcription factor. We performed targeted disruption of two Nrf3 exons coding for CNC homology, basic DNA-binding, and leucine zipper dimerization domains. Nrf3 null mice developed normally and revealed no obvious phenotypic differences compared to wild-type animals. Nrf3 ؊/؊ mice were fertile, and gross anatomy as well as behavior appeared normal. The mice showed normal age progression and did not show any apparent additional phenotype during their life span. We observed no differences in various blood parameters and chemistry values. We infected wild-type and Nrf3 ؊/؊ mice with acute lymphocytic choriomeningitis virus and found no differences in these animals with respect to their number of virus-specific CD8 and CD4 T cells as well as their B-lymphocyte response. To determine whether the mild phenotype of Nrf3 null animals is due to functional redundancy, we generated mice deficient in multiple CNC factors. Contrary to our expectations, an absence of Nrf3 does not seem to cause additional lethality in compound Nrf3 ؊/؊ /Nrf2 ؊/؊ and Nrf3 ؊/؊ /p45 ؊/؊ mice. We hypothesize that the role of Nrf3 in vivo may become apparent only after appropriate challenge to the mice.

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Section: Resultsmentioning

confidence: 99%

Complexity of CNC Transcription Factors As Revealed by Gene Targeting of the Nrf3 Locus

Derjuga¹,

Gourley

Holm

et al. 2004

Molecular and Cellular Biology

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“…Nevertheless, no effector cells were induced by this regimen. Interestingly, LCMV induced more pronounced expression of CD25, most likely because of Ag persistence due to viral replication, peaking between days 3 and 5 after infection (26,27).…”

Section: Up-regulation Of Activation Markers Despite the Absence Of Ementioning

confidence: 99%

Innate Immunity Together with Duration of Antigen Persistence Regulate Effector T Cell Induction

Storni¹,

Ruedl²,

Renner³

et al. 2003

The Journal of Immunology

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Proliferation of T cells is important for the expansion of specific T cell clones during immune responses. In addition, for the establishment of protective immunity against viruses, bacteria, and tumors, the expanded T cells must differentiate into effector T cells. Here we show that effector T cell generation is driven by activation of APCs and duration of antigenic stimulation. Adoptively transferred TCR-transgenic T cells extensively proliferated upon immunization. However, these T cells failed to differentiate into effector cells and died within 1 wk after immunization unless antigenic peptides persisted for >1 day or were presented by activated APCs. The induction of protective immunity in a nontransgenic system was more stringent, since activation of APCs or prolonged Ag persistence alone was not sufficient to drive immunity. In contrast, Ag had to be presented for several days by activated APCs to trigger protective T cell responses. Thus, activation of APCs and duration of Ag presentation together regulate the induction of protective T cell responses.

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“…injection of 2 ϫ 10 5 PFU of LCMV Armstrong. LCMV is a natural mouse pathogen, and the Armstrong strain is quickly cleared by the antiviral CD8 immune response that peaks 8 days postinfection (35,43,44). At various time points following infection, CD8 ϩ T cells from spleen and peripheral blood were analyzed for expression of ␤-gal in conjunction with markers for lymphocyte activation.…”

Section: ␤-Gal Marking Of Cd8 ϩ T Cells During An Immune Response To mentioning

confidence: 99%

A Transgenic Mouse Model Genetically Tags All Activated CD8 T Cells

Maris

Miller

Altman

et al. 2003

The Journal of Immunology

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Identifying and characterizing Ag-specific CD8+ T cells are central to the study of immunological memory. Although powerful strategies such as MHC tetramers and peptide-induced cytokine production assays exist for identifying Ag-specific CD8+ T cells, alternate strategies that are not dependent upon a priori knowledge of the immunodominant and subdominant antigenic epitopes, as well as the MHC background of the animal are of obvious utility. In this study, we present a transgenic mouse model that uses Cre-loxP recombination to permanently mark all activated CD8+ T cells with β-galactosidase. We used the lymphocytic choriomeningitis virus infection model to track the dynamics of the antiviral CD8+ T cell responses. We show that in this transgenic mouse model system, all of the antiviral effector and memory CD8+ T cells are contained within the β-gal-marked CD8+ T cell population.

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Virus and Immune Responses: Lymphocytic Choriomeningitis Virus as a Prototype Model of Viral Pathogenesis

Cited by 46 publications

References 0 publications

Complexity of CNC Transcription Factors As Revealed by Gene Targeting of the Nrf3 Locus

Complexity of CNC Transcription Factors As Revealed by Gene Targeting of the Nrf3 Locus

Innate Immunity Together with Duration of Antigen Persistence Regulate Effector T Cell Induction

A Transgenic Mouse Model Genetically Tags All Activated CD8 T Cells

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