Characterization of Effector Cells against B16 Melanoma in Mice Inoculated with Allogeneic Spleen Cells

Nishi, Yasuaki; Hosokawa, Tomokazu; Aoike, Akira; Han, Di; Takehara, Hiroshi; Kawai, Keiichi; Kamahora, Takeshi

doi:10.1111/j.1348-0421.1994.tb01767.x

Cited by 2 publications

(1 citation statement)

References 14 publications

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“…For depletion of T cells, mice were injected intravenously with 40 µg of anti-thy 1,2 (CD90) mAb (Cedarlane), anti-CD4 mAb (clone H129.19, rat IgG2a; PharMingen, San Diego, Calif., USA) or anti-CD8 mAb (clone 53-6.7, rat IgG2a; PharMingen), and for depletion for NK cells, 100 µl of anti-asialo GM1 antiserum (Wako Pure Chemical Industries Ltd., Osaka, Japan) diluted at 10/1 was injected into each mouse through the caudal vein, 1 day before tumor cell injection, according to the manufacturer’s instructions and previously published methods [25, 26, 27, 28]. …”

Section: Methodsmentioning

confidence: 99%

Inoculation of Human Interleukin-17 Gene-Transfected Meth-A Fibrosarcoma Cells Induces T Cell-Dependent Tumor-Specific Immunity in Mice

Hirahara

Nio²,

Sasaki³

et al. 2001

Oncology

111

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Objective: The biological activities of interleukin-17 (IL-17), a newly cloned cytokine, have not been fully elucidated. The present study was designed to assess the in vitro and in vivo effect of transfecting the IL-17 gene into tumor cells. Methods: A complementary DNA (cDNA) encoding human IL-17 (hIL-17) was obtained by polymerase chain reaction amplification from the human CD4+ T cell cDNA library and inserted into the plasmid pRc/cytomegalovirus to construct an expression vector for the hIL-17 gene. Murine Meth-A fibrosarcoma cells were transfected with the hIL-17 gene using the lipofectin method. The hIL-17 gene-expressing clone (Meth-A/IL-17) was selected and analyzed for cytokine expression by Northern blot. Results: There was no significant difference in the in vitro proliferation rate among parent Meth-A, cells transfected with vector alone and Meth-A/IL-17 cells. When the tumor cells were transplanted subcutaneously into BALB/c nude (nu+/nu+) mice, there was no difference in in vivo growth rates among the three cell lines. Challenge with tumor cells in conventional BALB/c mice, however, resulted in the rejection of Meth-A/IL-17 cells, but the other two lines did grow. After immunization with Meth-A/IL-17 cells, the mice were rechallenged by parent Meth-A or syngeneic MOPC-104E plasmacytoma cells; the immunized mice rejected the Meth-A cells, but not the MOPC-104E cells. Injecting the anti-thy 1,2 (CD90), anti-CD4 or anti-CD8 monoclonal antibody into conventional BALB/c mice resulted in the resumption of in vivo growth of Meth-A/IL-17 cells, but injecting the anti-asialo GM1 antibody did not. Furthermore, flow cytometric analysis demonstrated a significant increase in the expression of major histocompatibility complex (MHC) class I and class II antigens and lymphocyte function-associated antigen-1 on Meth-A/IL-17 cells. Conclusion: Meth-A cells transfected with the hIL-17 gene can induce tumor-specific antitumor immunity by augmenting the expression of MHC class I and II antigens, and both CD4+ and CD8+ T cells may play important roles in inducing antitumor immunity, suggesting the possibility of developing a tumor vaccine incorporating IL-17-transfected tumor cells.

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Section: Methodsmentioning

confidence: 99%

Inoculation of Human Interleukin-17 Gene-Transfected Meth-A Fibrosarcoma Cells Induces T Cell-Dependent Tumor-Specific Immunity in Mice

Hirahara

Nio²,

Sasaki³

et al. 2001

Oncology

111

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Immunological tolerance and tumor rejection in embryo-aggregated chimeric mice – Lessons for tumor immunity

Wagner

Holle

et al. 2008

BMC Cancer

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BackgroundRejection of transplanted tumors by the immune system is a rare event in syngeneic hosts, and is considered to be dependent on the local interaction of defensive immune reactions and tumor tolerance mechanisms. Here, we have enlisted the aid of a unique set of embryo-aggregated lineage chimeric mice derived from C57/BL6 and FVB donors to study the interplay between local and systemic tumor immunity and tolerance in rejection of mouse B16 melanoma cells, syngeneic to the C57/BL6 donor strain.MethodsTwo variants of embryo-aggregated chimeric mice with either variable or no contribution of C57-derived cells to their skin were generated by the fusion of different ratios of morula stage blastomers. Chimeric mice were analyzed for s.c. growth of B16 tumors in comparison to their respective donor strains as well as normal F1 hybrids, and the relative frequencies of cellular components of the immune system by FACS analysis of peripheral blood or lymph node cells.ResultsB16 tumors grew significantly faster in mice with full chimerism in their skin as compared to syngeneic C57 or semi-syngeneic C57 × FVB F1 hosts. In contrast, s.c. tumor growth was either absent or significantly reduced in chimeric mice lacking C57-derived cells in their skin, but tolerant to C57 tissue in other organs. Comparison of the relative frequencies of various immune cells in the periphery via FACS-analysis did not reveal any significant differences between the two types of chimeric mice with respect to their donor strains.ConclusionOur data suggest a complex interplay between mechanisms of local peripheral tolerance and innate antitumor mechanisms possibly involving NK cell allorecognition as a basis for the differential growth or rejection of B16 tumors in these unique chimeric mice, which we suggest to constitute a valuable new model system for the study of immune-mediated tumor rejection.

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Characterization of Effector Cells against B16 Melanoma in Mice Inoculated with Allogeneic Spleen Cells

Cited by 2 publications

References 14 publications

Inoculation of Human Interleukin-17 Gene-Transfected Meth-A Fibrosarcoma Cells Induces T Cell-Dependent Tumor-Specific Immunity in Mice

Inoculation of Human Interleukin-17 Gene-Transfected Meth-A Fibrosarcoma Cells Induces T Cell-Dependent Tumor-Specific Immunity in Mice

Immunological tolerance and tumor rejection in embryo-aggregated chimeric mice – Lessons for tumor immunity

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