Immunisation with modified HPV16 E7 genes against mouse oncogenic TC-1 cell sublines with downregulated expression of MHC class I molecules

Šmahel, Michal; Šíma, Pavel; Ludvı́ková, Viera; Marinov, Iuri; Pokorná, Dana; Vonka, V.

doi:10.1016/s0264-410x(02)00519-4

Cited by 68 publications

(82 citation statements)

References 57 publications

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“…Wu (Dr ChienFu Hong), Johns Hopkins University, Baltimore, MD, and TC-1/A9 tumour cell line, deficient in MHC class I molecules were used (18,19). As a second model, spontaneously metastasizing, HPV16-associated MK16/1/IIIABC (MK16) tumour cell line, also MHC class I deficient, was also utilized (19,20 5 cells/ml medium/48 h (7; Vonka and Sobotková, unpublished data). The cell lines were maintained in RPMI-1640 medium supplemented with 10% fetal calf serum, 2 mM L-glutamine and antibiotics (complete medium) and were cultured at 37˚C in a humified atmosphere with 5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

IL-12 immunotherapy of minimal residual disease in murine models of HPV16-associated tumours: induction of immune responses, cytokine production and kinetics of immune cell subsets

Indrová¹,

Bieblová²,

Bubenı́k³

et al. 2008

Int J Oncol

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Abstract.We have established animal models of HPV16-associated tumours with distinct levels of MHC class I expression. This model was used for examination of immune responses, production of cytokines and kinetics of immune cell subsets after IL-12 therapy of minimal residual tumour disease induced by CBA-4A (cyclophosphamide derivative) treatment. Upregulation of cytokine production was detected, compared to control animals without tumours. No differences in Th1/Th2 polarization of the immune responses after immunotherapy in animals bearing tumours with different surface expression of MHC class I molecules were observed. In the spleens of TC-1 (MHC class I + ) but not of TC-1/A9 (MHC class I -) treated tumour-bearing animals, the cytotoxic CD8 + cells detectable in 51 Cr microcytotoxicity assay, were found. In the spleens of TC-1/A9 but not of TC-1 tumourtreated animals, the NK activity measured as the lysis of NK-sensitive YAC-1 targets was detected. Down-regulation of the CD4 + and CD8 + subpopulations in spleens of tumourbearing animals were not restored after therapy. The percentage of CD25 + /CD4 + T regulatory (T reg ) cells in lymph nodes remained unchanged. The cytoreductive chemotherapy led to strong upregulation and accumulation of immunosuppressive immature myeloid Gr-1 + /CD11b + cells (IMC) in the spleens of treated animals. The accumulation of Gr-1 + /CD11b + cells was significantly decreased after subsequent IL-12 immunotherapy. These data suggest that elimination of IMC after IL-12 immunotherapy may be responsible for the improvement of antitumour responses after adjuvant IL-12 vaccination for the treatment of CMRTD.

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Section: Methodsmentioning

confidence: 99%

IL-12 immunotherapy of minimal residual disease in murine models of HPV16-associated tumours: induction of immune responses, cytokine production and kinetics of immune cell subsets

Indrová¹,

Bieblová²,

Bubenı́k³

et al. 2008

Int J Oncol

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“…HPV16-associated, non-metastasizing, MHC class I-positive cell line TC-1, moderately immunogenic in syngeneic B6 mice was obtained by in vitro co-transfection of murine lung C57BL/6 cells with HPV16 E6/E7 and activated human H-ras (G12V) oncogenes (16). TC-1/A9 tumour cell line, deficient in MHC class I molecules, represents tumour cell derivative which escaped from the selection pressure mediated by the specific immune response (17). Another E6/E7-expressing MHC class I-deficient, spontaneously metastasizing cell line MK16/1/IIIABC (MK16), moderately immunogenic in syngeneic mice, was developed by in vitro co-transfection of murine C57BL/6 kidney cells with a mixture of plasmids carrying activated H-ras oncogene (plasmid pEJ6.6), HPV16 E6/E7 genes (plasmid p16HHMo) and neomycin resistance gene (plasmid pAG60) (18,19).…”

Section: Introductionmentioning

confidence: 99%

NK1.1+ cells are important for the development of protective immunity against MHC I-deficient, HPV16-associated tumours

Indrová

Šímová²,

Bieblová³

et al. 2010

Oncol Rep

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“…Wu (Johns Hopkins University, Baltimore) were prepared by the transformation of C57BL/6 primary mouse lung epithelial cells by HPV16 E6/E7 oncogenes and the activated H-ras oncogene (27). They were maintained as previously described (31). In the present experiments cells from the 3rd passage, derived from a large frozen stock, were used.…”

Section: Methodsmentioning

confidence: 99%

Human hair follicle and interfollicular keratinocyte reactivity to mouse HPV16-transformed cells: An in vitro study

Smetana¹,

Dvořánková²,

Lacina³

et al. 2008

Oncol Rep

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Abstract. The role of stem cells in cancer formation and spreading has been established. As with normal tissue, the cancer stem cells need a special microenvironment to support their growth. This microenvironment may be represented by the tumor stroma. One of the possible ways of tumor stromal formation is the epithelial-mesenchymal transition of tumor epithelium. Following this mechanism, stromal cells must share the basic genetic alterations with the tumor cells. In an attempt to create a system capable of testing some aspects of the mesenchymal cell-keratinocyte interactions, we studied the effects of the fibroblastoid mouse TC-1 cells that were prepared by the introduction of human papillomavirus type 16 (HPV16) genes E6 and E7 to lung epithelial cells on the phenotype of normal human interfollicular and hair follicle keratinocytes. From this point of view, they may resemble stromal cells formed by the epithelial-mesenchymal transition of cells from HPV-induced squamous cell carcinoma. In contrast to 3T3 murine embryonic fibroblasts which were used as control cells, TC-1 cells influenced not only the size of the keratinocytes and the shape of their colonies, but also induced the expression of keratins 8 and 19 and vimentin. In conclusion, TC-1 cells exhibited a marked biological activity by influencing the behavior of the normal human follicular and intefollicular keratinocytes. This observation is compatible with the hypothesis that stromal cells play an important role in tumor progression and spreading.

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Immunisation with modified HPV16 E7 genes against mouse oncogenic TC-1 cell sublines with downregulated expression of MHC class I molecules

Cited by 68 publications

References 57 publications

IL-12 immunotherapy of minimal residual disease in murine models of HPV16-associated tumours: induction of immune responses, cytokine production and kinetics of immune cell subsets

IL-12 immunotherapy of minimal residual disease in murine models of HPV16-associated tumours: induction of immune responses, cytokine production and kinetics of immune cell subsets

NK1.1+ cells are important for the development of protective immunity against MHC I-deficient, HPV16-associated tumours

Human hair follicle and interfollicular keratinocyte reactivity to mouse HPV16-transformed cells: An in vitro study

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