Cytokine-mediated modulation of HLA-class II, ICAM-1, LFA-3 and tumor-associated antigen profile of melanoma cells. Comparison with anti-proliferative activity by rIL1-β, rTNF-α, rIFN-γ, rIL4 and their combinations

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Abstract

Nine different human melanomas and 16 clones, isolated from 2 of them, were characterized for susceptibility to rIL1-β-, rIL4-, rTNF-α- and rIFN-γ-mediated effects on proliferation and surface expression of class-II HLA (DR and DP), ICAM-1 and LFA-3 molecules and of 3 tumor-associated antigens (recognized by MAb 763.74T, 149.53 and R24). In spite of marked inter- and intra-tumor heterogeneity for susceptibility to the effects of each cytokine, the most frequent upregulation was induced on the HLA class-II antigens by rIFN-γ and on adhesion molecules by rIFN-γ, rTNF-α and rIL1-β, while tumor-associated antigens were often down-modulated by rIFN-γ. Tumor heterogeneity was also evident on tumor-cell proliferation with an apparent hierarchy in the frequency and extent of inhibitory effects: rIFN-γ > rTNF-α > rIL1-β = rIL4. Combinations of 2 cytokines resulted in rare and limited changes in the antigenic profile in comparison to the effects seen with single factors, while the combination of rTNF-α and rIFN-γ resulted in significant synergistic antiproliferative effects on most tumor cells and clones. Taken together, these results indicate that single cytokines can profoundly affect the antigenic profile of melanoma cells, while strong tumor-growth inhibition is often achieved by combinations of 2 cytokines acting in synergism.

Original languageEnglish
Pages (from-to)334-341
Number of pages8
JournalInternational Journal of Cancer
Volume45
Issue number2
Publication statusPublished - 1990

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CD58 Antigens
Neoplasm Antigens
Intercellular Adhesion Molecule-1
Melanoma
Cytokines
Neoplasms
Clone Cells
HLA-DP Antigens
Histocompatibility Antigens Class II
HLA-DR Antigens
HLA Antigens
Up-Regulation
Cell Proliferation
Growth

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

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title = "Cytokine-mediated modulation of HLA-class II, ICAM-1, LFA-3 and tumor-associated antigen profile of melanoma cells. Comparison with anti-proliferative activity by rIL1-β, rTNF-α, rIFN-γ, rIL4 and their combinations",
abstract = "Nine different human melanomas and 16 clones, isolated from 2 of them, were characterized for susceptibility to rIL1-β-, rIL4-, rTNF-α- and rIFN-γ-mediated effects on proliferation and surface expression of class-II HLA (DR and DP), ICAM-1 and LFA-3 molecules and of 3 tumor-associated antigens (recognized by MAb 763.74T, 149.53 and R24). In spite of marked inter- and intra-tumor heterogeneity for susceptibility to the effects of each cytokine, the most frequent upregulation was induced on the HLA class-II antigens by rIFN-γ and on adhesion molecules by rIFN-γ, rTNF-α and rIL1-β, while tumor-associated antigens were often down-modulated by rIFN-γ. Tumor heterogeneity was also evident on tumor-cell proliferation with an apparent hierarchy in the frequency and extent of inhibitory effects: rIFN-γ > rTNF-α > rIL1-β = rIL4. Combinations of 2 cytokines resulted in rare and limited changes in the antigenic profile in comparison to the effects seen with single factors, while the combination of rTNF-α and rIFN-γ resulted in significant synergistic antiproliferative effects on most tumor cells and clones. Taken together, these results indicate that single cytokines can profoundly affect the antigenic profile of melanoma cells, while strong tumor-growth inhibition is often achieved by combinations of 2 cytokines acting in synergism.",
author = "R. Mortarini and F. Belli and G. Parmiani and A. Anichini",
year = "1990",
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T1 - Cytokine-mediated modulation of HLA-class II, ICAM-1, LFA-3 and tumor-associated antigen profile of melanoma cells. Comparison with anti-proliferative activity by rIL1-β, rTNF-α, rIFN-γ, rIL4 and their combinations

AU - Mortarini, R.

AU - Belli, F.

AU - Parmiani, G.

AU - Anichini, A.

PY - 1990

Y1 - 1990

N2 - Nine different human melanomas and 16 clones, isolated from 2 of them, were characterized for susceptibility to rIL1-β-, rIL4-, rTNF-α- and rIFN-γ-mediated effects on proliferation and surface expression of class-II HLA (DR and DP), ICAM-1 and LFA-3 molecules and of 3 tumor-associated antigens (recognized by MAb 763.74T, 149.53 and R24). In spite of marked inter- and intra-tumor heterogeneity for susceptibility to the effects of each cytokine, the most frequent upregulation was induced on the HLA class-II antigens by rIFN-γ and on adhesion molecules by rIFN-γ, rTNF-α and rIL1-β, while tumor-associated antigens were often down-modulated by rIFN-γ. Tumor heterogeneity was also evident on tumor-cell proliferation with an apparent hierarchy in the frequency and extent of inhibitory effects: rIFN-γ > rTNF-α > rIL1-β = rIL4. Combinations of 2 cytokines resulted in rare and limited changes in the antigenic profile in comparison to the effects seen with single factors, while the combination of rTNF-α and rIFN-γ resulted in significant synergistic antiproliferative effects on most tumor cells and clones. Taken together, these results indicate that single cytokines can profoundly affect the antigenic profile of melanoma cells, while strong tumor-growth inhibition is often achieved by combinations of 2 cytokines acting in synergism.

AB - Nine different human melanomas and 16 clones, isolated from 2 of them, were characterized for susceptibility to rIL1-β-, rIL4-, rTNF-α- and rIFN-γ-mediated effects on proliferation and surface expression of class-II HLA (DR and DP), ICAM-1 and LFA-3 molecules and of 3 tumor-associated antigens (recognized by MAb 763.74T, 149.53 and R24). In spite of marked inter- and intra-tumor heterogeneity for susceptibility to the effects of each cytokine, the most frequent upregulation was induced on the HLA class-II antigens by rIFN-γ and on adhesion molecules by rIFN-γ, rTNF-α and rIL1-β, while tumor-associated antigens were often down-modulated by rIFN-γ. Tumor heterogeneity was also evident on tumor-cell proliferation with an apparent hierarchy in the frequency and extent of inhibitory effects: rIFN-γ > rTNF-α > rIL1-β = rIL4. Combinations of 2 cytokines resulted in rare and limited changes in the antigenic profile in comparison to the effects seen with single factors, while the combination of rTNF-α and rIFN-γ resulted in significant synergistic antiproliferative effects on most tumor cells and clones. Taken together, these results indicate that single cytokines can profoundly affect the antigenic profile of melanoma cells, while strong tumor-growth inhibition is often achieved by combinations of 2 cytokines acting in synergism.

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