γ-Ray irradiation induces B7.1 costimulatory molecule neoexpression in various murine tumor cells

Morel, Anthony; Fernandez, Nadine; Coste, Anne; Haddada, Hédi; Viguier, Mireille; Polla, Barbara S.; Antoine, B; Kahn, Axel

doi:10.1007/s002620050488

Cited by 30 publications

(27 citation statements)

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“…A processed form of CD74 has been identified as a secreted factor that inhibits IL-2 production by activated T cells (22). The ability of CD28 signaling to reciprocally regulate antiproliferative and stimulatory genes (e.g., repression of BCL6 and induction of IL-2) suggests that multiple mechanisms function in concert to limit T cell proliferation in the absence of a costimulatory signal delivered by a professional antigen-presenting cell or encountered in the context of a potential threat or stress (23).…”

Section: ϫ5mentioning

confidence: 99%

Genomic expression programs and the integration of the CD28 costimulatory signal in T cell activation

Diehn

Alizadeh

Rando

et al. 2002

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

307

264

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Optimal activation of T cells requires effective occupancy of both the antigen-specific T cell receptor and a second coreceptor such as CD28. We used cDNA microarrays to characterize the genomic expression program in human peripheral T cells responding to stimulation of these receptors. We found that CD28 agonists alone elicited few, but reproducible, changes in gene expression, whereas CD3 agonists elicited a multifaceted temporally choreographed gene expression program. The principal effect of simultaneous engagement of CD28 was to increase the amplitude of the CD3 transcriptional response. The induced genes whose expression was most enhanced by costimulation were significantly enriched for known targets of nuclear factor of activated T cells (NFAT) transcription factors. This enhancement was nearly abolished by blocking the nuclear translocation of NFATc by using the calcineurin inhibitor FK506. CD28 signaling promoted phosphorylation, and thus inactivation, of the NFAT nuclear export kinase glycogen synthase kinase-3 (GSK3), coincident with enhanced dephosphorylation of NFATc proteins. These results provide a detailed picture of the transcriptional program of T cell activation and suggest that enhancement of transcriptional activation by NFAT, through inhibition of its nuclear export, plays a key role in mediating the CD28 costimulatory signal

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Section: ϫ5mentioning

confidence: 99%

Genomic expression programs and the integration of the CD28 costimulatory signal in T cell activation

Diehn

Alizadeh

Rando

et al. 2002

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

307

264

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“…14,15 Thus, irradiation profoundly alters the pattern of expression of transduced and untransduced cells. In our experiments, enhancement of expression occurred with a reporter gene and genes with potential therapeutic interest in acute leukemia including secreted (GM-CSF) and cell surface molecules (CD80).…”

Section: Discussionmentioning

confidence: 99%

“…Cells were also exposed to oxidative stress and heat shock as previously described. 14,15 Briefly H 2 O 2 was added to cultured medium at 1 mM final concentration and cells were further incubated for 18 h before transgene expression analysis. In some experiments, N-acetyl-cystein (NAC) was added at 25 mM 1 h before irradiation or oxidative stress induction to ensure inhibition of NF-kB activation.…”

Section: Gene Transfermentioning

confidence: 99%

γ-Irradiation enhances transgene expression in leukemic cells

et al. 2003

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“…Moreover, ␥-irradiation was reported to up-regulate B7-1 surface expression on primary cultures of human acute myeloid leukemic cell samples (29). Subsequent attempts to mimic the effect of ␥-irradiation on B7-1 surface expression with H 2 O 2 revealed that while exposure of the murine AT3F hepatoma to ␥-irradiation resulted in a profound elevation in B7-1 mRNA and surface expression, exposure of these tumor cells for 60 min to H 2 O 2 at a concentration of 2 mM, but not 1 mM, resulted in a slight elevation in B7-1 mRNA and surface expression (27). In contrast, exposure of the murine DA13b myeloid leukemic cell line for 60 min to 1 mM H 2 O 2 (the only conditions reported) resulted in a substantial elevation in B7-1 surface expression, although not as profound as following exposure to 25 Gy ␥-irradiation (29).…”

Section: Discussionmentioning

confidence: 99%

“…We (15), as well as others (27,29,44), have recently shown that B7-1 surface expression can be selectively up-regulated on several different murine tumor cell lines, by exposing the tumor cells to a different anticancer modality, i.e., ␥-irradiation. Moreover, ␥-irradiation was reported to up-regulate B7-1 surface expression on primary cultures of human acute myeloid leukemic cell samples (29).…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Melphalan-Induced B7-1 Gene Expression in P815 Tumor Cells

Donepudi

Raychaudhuri

Bluestone

et al. 2001

The Journal of Immunology

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We have previously shown that exposure of P815 tumor cells to melphalan (l-phenylalanine mustard; l-PAM) leads to up-regulation of B7-1 surface expression, and this l-PAM-induced up-regulation requires de novo RNA synthesis and is associated with accumulation of B7-1 mRNA. Here we show that the effect of l-PAM on B7-1 surface expression can be mimicked by exposing P815 tumor cells to oxidative stress but not to heat shock. Moreover, the antioxidant N-acetyl-l-cysteine prevented the l-PAM-induced accumulation of B7-1 mRNA in P815 tumor cells, suggesting that reactive oxygen species are involved in the transcriptional regulation of l-PAM-induced B7-1 gene expression. Although AP-1 and NF-κB are regarded as redox-sensitive transcription factors and the promoter/enhancer region of the B7-1 gene contains an AP-1 and an NF-κB binding site, exposure of P815 tumor cells to l-PAM led to rapid and transient activation only of NF-κB, but not AP-1, that bound specifically to a probe containing the respective binding site in the murine or human B7-1 gene. Moreover, exposure of P815 tumor cells to a cell-permeable peptide that selectively inhibits NF-κB activation by blocking the activation of the IκB-kinase complex was found to inhibit the l-PAM-induced B7-1 mRNA accumulation, indicating that NF-κB activation is essential for the l-PAM-induced B7-1 gene expression. Taken together, these results indicate that l-PAM leads to activation of B7-1 gene expression by activating NF-κB via a pathway that involves reactive oxygen species.

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γ-Ray irradiation induces B7.1 costimulatory molecule neoexpression in various murine tumor cells

Cited by 30 publications

References 0 publications

Genomic expression programs and the integration of the CD28 costimulatory signal in T cell activation

Genomic expression programs and the integration of the CD28 costimulatory signal in T cell activation

γ-Irradiation enhances transgene expression in leukemic cells

Mechanism of Melphalan-Induced B7-1 Gene Expression in P815 Tumor Cells

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