Unique T Cell Antagonist Properties of the Exact Self-Correlate of a Peptide Antigen Revealed by Self-Substitution of Non-Self-Positions in the Peptide Sequence

Schountz, Tony; Kasselman, Joel P.; Ford, Stephanie R.; Murray, Joseph S.

doi:10.1006/cimm.1996.0066

Cited by 5 publications

(7 citation statements)

References 3 publications

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“…It is possible that during the coadaptation of hantaviruses to their rodent reservoirs, natural selection favored rodents able to produce viral polypeptides that limited T cell signaling through the T cell receptor. In other T cell peptide studies using inbred laboratory house mice, poor peptide binding to MHC molecules has been shown to reduce the proliferative magnitude and cytokine profiles of T cell responses (49)(50)(51)(52). Whereas high-density peptides induced strong proliferation and Th1 cytokine responses, low-density peptides induced weak proliferation and Th2 cytokines.…”

Section: Discussionmentioning

confidence: 98%

“…Supporting this contention, de Carvalho Nicacio et al found MHC-specific differences in proliferation magnitude to recombinant Puumala virus N-Ag in inbred strains of laboratory house mice (48). In addition, some viral peptides are antagonistic to T cell responses, such that they can impact effector T cell maturation (53)(54)(55). Such antagonism can lead to regulatory T cell activation and bystander suppression of an inflammatory immune response (56).…”

Section: Discussionmentioning

confidence: 99%

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Regulatory T cell-like responses in deer mice persistently infected with Sin Nombre virus

Schountz

Prescott²,

Cogswell³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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107

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Hantavirus cardiopulmonary syndrome is a zoonotic illness associated with a systemic inflammatory immune response, capillary leak, noncardiogenic pulmonary edema, and shock in humans. Cytokines, including TNF, IFN-␥, and lymphotoxin, are thought to contribute to its pathogenesis. In contrast, infected rodent reservoirs of hantaviruses experience few or no pathologic changes and the host rodent can remain persistently infected for life. Generally, it is unknown why such dichotomous immune responses occur between humans and reservoir hosts. Thus, we examined CD4 ؉ T cell responses from one such reservoir, the deer mouse (Peromy-

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Regulatory T cell-like responses in deer mice persistently infected with Sin Nombre virus

Schountz

Prescott²,

Cogswell³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

107

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“…Single-cell suspensions of tumors were made by gently disrupting tumors in Hank's balanced salt solution (HBSS; Life Technologies, Bethesda, MD, USA; Schountz et al, 1996). Cells were resuspended in tumor medium at 10 6 cells/ml, then tissue culture grade DMSO (Sigma) was added to 10% v/v.…”

Section: Tumor Processingmentioning

confidence: 99%

“…Antibodies used were to CD4 (RM4-4), CD8a (53-6.7), CD19 (1D3), CD24 (M1/69), CD34 (RAM34/49E8), CD38 (90), CD117 (2B8), B220 (cat #553086), and Thy1 (cat #553013). Cells were washed twice, then fixed in 1% paraformaldehyde, and 10 000 events collected with a FACStar flow cytometer (Becton-Dickinson) as described previously (Schountz et al, 1996).…”

Section: Flow Cytometrymentioning

confidence: 99%

Evi3, a zinc-finger protein related to EBFAZ, regulates EBF activity in B-cell leukemia

et al. 2004

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Retroviral insertions that activate proto-oncogenes are a primary cause of tumors in certain strains of mice. The AKXD recombinant inbred mice are predisposed to a variety of leukemias and lymphomas as a result of viral integration. One common insertion site, the ecotropic viral insertion site 3 (Evi3), has been implicated in most B-cell tumors in the AKXD-27 strain. The Evi3 gene encodes a zinc-finger protein with sequence similarity to the Early B-cell Factor-Associated Zinc-finger gene (EBFAZ). We show that the Evi3 gene is overexpressed in several tumors with viral insertions at Evi3, which results in the upregulation of Early B-cell Factor (EBF)-target gene expression, suggesting that Evi3 modulates EBF activity. Reconstitution of primary leukemia cells showed that these tumors express high densities of the Bcell surface proteins CD19 and CD38, which are EBF targets. Using a transactivation assay, we show that the terminal six zinc-fingers of Evi3 are required for modification of EBF activity. This is the first evidence that Evi3 expression in tumors alters the level of EBF target genes, and the first characterization of the Evi3 protein domains required for modulation of EBF activity. Further, these data imply that Evi3 misexpression initiates tumorigenesis by perturbing B-cell development via an interaction with EBF.

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“…Among the population of peptides presented in the periphery, there may exist ligands that could function as antagonists. Indeed, exogenously added peptides derived from self proteins have been shown to antagonize a cytotoxic T lymphocyte line (9) and a T cell hybrid (10) in vitro. It has not been established, however, if endogenous proteins containing antagonist peptides can modulate a T cell response to a foreign antigen in vivo.…”

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confidence: 99%

In vivoantagonism of a T cell response by an endogenously expressed ligand

Basu

Williams

Allen

1998

Proc. Natl. Acad. Sci. U.S.A.

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Unique T Cell Antagonist Properties of the Exact Self-Correlate of a Peptide Antigen Revealed by Self-Substitution of Non-Self-Positions in the Peptide Sequence

Cited by 5 publications

References 3 publications

Regulatory T cell-like responses in deer mice persistently infected with Sin Nombre virus

Regulatory T cell-like responses in deer mice persistently infected with Sin Nombre virus

Evi3, a zinc-finger protein related to EBFAZ, regulates EBF activity in B-cell leukemia

In vivoantagonism of a T cell response by an endogenously expressed ligand

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