Interleukin-2 augmented activation of tumor associated macrophage plays the main role in MHC class I in vivo induction in tumor cells that are MHC negative in vitro

  • Authors:
    • Guan-Feng Ouyang
    • Masanao Saio
    • Tatsuhiko Suwa
    • Hisashi Imai
    • Jiro Nakagawa
    • Kenichi Nonaka
    • Naoki Umemura
    • Mika Kijima
    • Tsuyoshi Takami
  • View Affiliations

  • Published online on: May 1, 2006     https://doi.org/10.3892/ijo.28.5.1201
  • Pages: 1201-1208
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Abstract

The contribution of tumor associated macrophage (TAM) to the induction of major histocompatibility complex (MHC) class I expression in vivo has not been reported precisely. In this study, we utilized Interleukin-2 (IL-2) cDNA-introduced B16 melanoma cells (B16/IL-2) and vehicle-alone control cells (B16/mock) to examine whether TAM could contribute to the induction of MHC class I on B16 cells in vivo. Interestingly, although B16/mock and B16/IL-2 did not express MHC class I in vitro, MHC class I was strongly expressed in vivo in B16/IL-2 in comparison to B16/mock. Although in vivo treatment of anti-NK1.1 antibody abolished MHC expression in B16/mock in vivo, the same treatment did not influence MHC expression in B16/IL-2. Interestingly, both anti-asialo GM1 and anti-CD11b treatment strongly decreased MHC expression in B16/IL-2. TAM expressed both asialo GM1 and CD11b antigen, and TAM recovered from B16/IL-2 produced interferon γ (IFNγ) 6 times more than that from B16/mock. In addition, TAM recovered from B16/IL-2 secreted 33.64 times more IFNγ in response to in vitro administration of IL-2. Therefore, we checked whether or not IL-2 could influence the expression of IL-2 receptors. TAM recovered from IL-2 expressed middle affinity receptor of IL-2 (CD122 and CD132) while that from B16/mock expressed low affinity receptor (CD25 and CD132). Finally, we observed that B16 cells became apoptotic with IFNγ treatment in vitro. These results suggested that IL-2 augmented activation of TAM would play the main role in induction of the MHC class I molecule through secretion of IFNγ, and would contribute to the IFNγ-mediated apoptosis induction in tumor cells.

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May 2006
Volume 28 Issue 5

Print ISSN: 1019-6439
Online ISSN:1791-2423

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APA
Ouyang, G., Saio, M., Suwa, T., Imai, H., Nakagawa, J., Nonaka, K. ... Takami, T. (2006). Interleukin-2 augmented activation of tumor associated macrophage plays the main role in MHC class I in vivo induction in tumor cells that are MHC negative in vitro. International Journal of Oncology, 28, 1201-1208. https://doi.org/10.3892/ijo.28.5.1201
MLA
Ouyang, G., Saio, M., Suwa, T., Imai, H., Nakagawa, J., Nonaka, K., Umemura, N., Kijima, M., Takami, T."Interleukin-2 augmented activation of tumor associated macrophage plays the main role in MHC class I in vivo induction in tumor cells that are MHC negative in vitro". International Journal of Oncology 28.5 (2006): 1201-1208.
Chicago
Ouyang, G., Saio, M., Suwa, T., Imai, H., Nakagawa, J., Nonaka, K., Umemura, N., Kijima, M., Takami, T."Interleukin-2 augmented activation of tumor associated macrophage plays the main role in MHC class I in vivo induction in tumor cells that are MHC negative in vitro". International Journal of Oncology 28, no. 5 (2006): 1201-1208. https://doi.org/10.3892/ijo.28.5.1201