Rejection of B16 melanoma induced by expression of a transfected major histocompatibility complex class I gene.

Tanaka, Kenichi; Gorelik, Elieser; Watanabe, Motoó; Hozumi, Nobumichi; Jay, Gilbert

doi:10.1128/mcb.8.4.1857

Cited by 62 publications

(41 citation statements)

References 30 publications

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“…Indeed, APC pulsed with B16-derived peptide epitopes are capable of eliciting specific CTL reactions directed against B16 melanoma both in vitro [24] and in vivo [25]. Furthermore, the transfection of B16 with the K b molecule converts it into a strongly immunogenic tumor in vivo [26] and renders it susceptible to rejection by immunocompetent mice [27]. Likewise, stably transfected B16 clones expressing the heat shock protein Hsp65, a "molecular chaperone," manifest significantly elevated levels of the MHC class I molecule and are more easily lysed by alloreactive CTL [28].…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effect of the polyinosinic‐polycytidylic acid/cationic liposome on the progression of murine B16F10 melanoma

et al. 2006

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Cellular proteins, retinoic acid inducible gene‐I and Toll‐like receptor 3, sense dsRNA including polyinosinic‐polycytidylic acid (PIC) to stimulate innate immune response. The local administration of PIC has been demonstrated to be effective in anti‐tumor immunotherapy. However, the effects of PIC delivered cross the cell membrane have not yet been examined. To address this issue, we used a complex of PIC and cationic liposome (PIC liposome) and examined its anti‐tumor effects in vitro and in vivo. PIC liposome could directly suppress the growth of B16F10 melanoma in vitro and repeated peritumoral injections of PIC liposome inhibited melanoma growth in a dose‐dependent manner. This treatment induced tyrosinase‐related protein‐2 (TRP‐2)‐tetramer+ CD8+ cells in the lymph nodes. As the mechanism for its anti‐tumor immune response, we showed that the intradermal injection of PIC liposome induced the maturation of dendritic cells (DC). Moreover, the intratumoral injection of immature DC after treatment with PIC liposome significantly increased the number of TRP‐2‐specific IFN‐γ‐producing cells in the lymph nodes as well as spleen, which resulted in an augmentation of the anti‐tumor immune response. These studies demonstrate the potential of peritumoral injection of PIC liposome as immunotherapy for malignant melanoma.

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Section: Discussionmentioning

confidence: 99%

Inhibitory effect of the polyinosinic‐polycytidylic acid/cationic liposome on the progression of murine B16F10 melanoma

et al. 2006

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“…C57BL͞6 and BALB͞c mice, 8-to 12-wk-old, were obtained from Janvier (Laval, France). The Bosc23-packaging cell line (16) was from American Type Culture Collection, and the tumor cell lines MCA205 (17) and CL8.1 (18) were gifts from L. Zitvogel (Institut Gustave Roussy, Villejuif, France) and E. Gorelik (University of Pittsburgh, Pittsburgh, PA), respectively. Culture conditions were as indicated in the corresponding references.…”

Section: Methodsmentioning

confidence: 99%

Tumor cells expressing a retroviral envelope escape immune rejectionin vivo

Mangeney

Heidmann²

1998

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

115

119

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A model system for the in vivo control of tumor cell proliferation by the immune system has been used to assay for the possible immunosuppressive activity of retroviral proteins. Expression vectors for the entire or the transmembrane subunit of the Moloney murine leukemia virus envelope protein were constructed, as well as control vectors for irrelevant transmembrane proteins-or no protein. They were introduced either into MCA205 murine tumor cells, which do not proliferate upon s.c. injection into an allogeneic host, or into CL8.1 murine tumor cells, which overexpress class I antigens and are rejected in a syngeneic host. In both cases, expression of the complete envelope protein or of the transmembrane subunit resulted in tumor growth in vivo, with no effect of control vectors. Tumor cell growth results from inhibition of the host immune response, as the envelope-dependent effect was no more observed for MCA205 cells in syngeneic mice or for CL8.1 cells in xirradiated mice. This inhibition is local because it is not observed at the level of control tumor cells injected contralaterally. These results suggest a noncanonical function of retroviral envelopes in the ''penetrance'' of viral infections, as well as a possible involvement of the envelope proteins of endogenous retroviruses in tumoral processes.

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“…BL6-8 and BL6-2 clones were also transfected with the p191-6 plasmid, which contains the entire H-2K agene cloned into the HindlII sites of pBR322 (Gorelik et al, 1991;Kim et al, 1994), or with the plasmids containing the genomic H-2D a or H-2L agene with the homogenous promoter (Kim et al, 1994). BL6-8 cells were also transfected with the pRSV plasmid containing both the 8"4 kb IAa k and 10 kb IAc~ k sequences of the class II H-2IA k gene (Tanaka et al, 1988). BL6-8 and BL6-2 ceils transfected with the class I or class [I MHC genes were cotransfected with the nea gene using Lipofectin reagent.…”

Section: Methodsmentioning

confidence: 99%

“…The BL6 melanoma subline was cloned and two clones, BL6-8 (H-2K b-, H-2Db+) and BL6-2 (H-2K b-, H-2D b-) were used as recipients of H-2 class I gene transfection. As detailed previously, BLb-8 or BL6-2 cells were transfected with the H-2K b genomic fragment subdoned into the SalI site of pTCF (Tanaka et aL, 1988;Gorelik et al, i991;Kim eta]., 1994). BL6-8 and BL6-2 clones were also transfected with the p191-6 plasmid, which contains the entire H-2K agene cloned into the HindlII sites of pBR322 (Gorelik et al, 1991;Kim et al, 1994), or with the plasmids containing the genomic H-2D a or H-2L agene with the homogenous promoter (Kim et al, 1994).…”

Section: Methodsmentioning

confidence: 99%

Loss of intracisternal A-type retroviral particles in BL6 melanoma cells transfected with MHC class I genes

Müller²,

Rao³

et al. 1996

Journal of General Virology

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Electron microscopy of B16 melanoma and its sublines revealed that these cells produce numerous intracisternal A-type retroviral particles (lAPs). To identify and sequence the melanoma-associated lAPs of C57BL/6 mice, a cDNA library was constructed from lAP-producing BL6-8 cell RNA and screened using MIA14 lAP DNA as a probe. A 6.8 kb mRNA was identified that represents the full-length message for a new subfamily of lAP, termed MelAP. The melanoma-derived lAP cDNA showed high similarity to MIA14 with major differences in the LTR. A nine base motif of the R region showed that this lAP differs from other previously sequenced lAPs. Analysis of the individual clones from BL6 melanoma revealed that lAPs were produced only in the clones that failed to express H-2K b molecules. No lAPs were found in the melanoma clones that expressed endogenous H-2K b. To analyse further the association between MHC class I genes and lAP production, the H-2Kb-negative clones of BL6 melanoma were transfected with various H-2 genes. Transfection of the H-2K b or H-2K d, but not H-2D d or H-2L d genes resulted in the elimination of lAPs.Northern blot analysis revealed that loss of lAPs in the H-2K gene-transfected BL6 melanoma cells was due to lack of lAP transcripts. Elimination of lAPs in the H-2Kb-positive BL6 melanoma cells was also accompanied by alterations in expression of various cellular genes and changes of their phenotypic properties.

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Rejection of B16 melanoma induced by expression of a transfected major histocompatibility complex class I gene.

Cited by 62 publications

References 30 publications

Inhibitory effect of the polyinosinic‐polycytidylic acid/cationic liposome on the progression of murine B16F10 melanoma

Inhibitory effect of the polyinosinic‐polycytidylic acid/cationic liposome on the progression of murine B16F10 melanoma

Tumor cells expressing a retroviral envelope escape immune rejectionin vivo

Loss of intracisternal A-type retroviral particles in BL6 melanoma cells transfected with MHC class I genes

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