Growth and metastasis in allogeneic hosts. Lack of H-2-negative or somatic hybrid variant selection

C. De Giovanni, P. L. Lollini, G. Nicoletti, B. Del Re, K. Scotlandi, G. Prodi, P. Nanni

Research output: Contribution to journalArticlepeer-review

Abstract

In vitro cultured B16 melanoma cells, which were previously found to have an impaired expression of H-2Kb and Db (as evaluated by antisera absorption assay), were used to study growth and metastasis in allogeneic mice in relation to H-2 expression. The possible emergence of somatic hybrids with host cells was also examined. B16-A cells grown subcutaneously in allogeneic BALB/c mice (H-2(d)) did not show a lack of H-2b expression, nor the acquirement of H-2(d) antigens was found. Spontaneous lung metastases were found in about 30% of BALB/c mice with progressing B16 tumor. Single lung metastases showed higher H-2b levels than cells from the respective tumors, and did not express host H-2 antigens. Tumor take was concomitant to the rise of an anti-H-2b humoral response: disease outcome was independent from the serum titer. B16-A cells injected intravenously in BALB/c mice gave rise to lung colonies; different colonies showed a wide range of H-2b antigens levels and no H-2(d) expression. Lung colonization capacity in normal allogeneic BALB/c mice was significantly higher than in syngeneic C57BL/6 mice. Both syngeneic and allogeneic mice, when pretreated with cyclophosphamide (CY) to reduce natural killer cell activity, showed a significant increase in lung colonization by B16-A cells. CY-treated C57BL/6 mice showed significantly higher numbers of lung colonies than CY-treated BALB/c mice. In conclusion B16 growth and metastasis in the allogeneic environment do not seem to be determined by a selection of H-2-negative variants or by the emergence of somatic hybrids with host cells.

Original languageEnglish
Pages (from-to)153-162
Number of pages10
JournalExperimental and Clinical Immunogenetics
Volume4
Issue number3
Publication statusPublished - 1987

ASJC Scopus subject areas

  • Genetics
  • Immunology
  • Genetics(clinical)

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