Class I major histocompatibility complex enhancement by recombinant leukocyte interferon in the peripheral blood mononuclear cells and plasma of melanoma patients

Patrizio Giacomini, Rocco Fraioli, Anna Maria Calabro, Franco Di Filippo, Pier Giorgio Natali

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

In vivo administration of escalation doses of recombinant α-Interferon (IFN-α) during a phase I trial in malignant melanoma patients caused dose-dependent increases in the mRNA accumulation, synthesis, steady state cellular content, and plasma membrane expression of class I major histocompatibility complex molecules in peripheral blood mononuclear cells. In addition, circulating levels of class I molecules were also enhanced. These findings show that (a) antigenic enhancement by biomodifiers may occur in vivo, in humans and (b) the mechanism of class I major histocompatibility complex enhancement by IFN-α is similar in vitro and in vivo. Furthermore, because peripheral blood mononuclear cells of different melanoma patients display different susceptibility to IFN-α, the entity of their antigenic modulation may represent a useful parameter to evaluate the efficacy of different therapeutic regimens and/ or assess the individual susceptibility to the molecular changes induced by IFN-α.

Original languageEnglish
Pages (from-to)652-656
Number of pages5
JournalCancer Research
Volume51
Issue number2
Publication statusPublished - Jan 15 1991

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Major Histocompatibility Complex
Interferon-alpha
Melanoma
Blood Cells
Antigenic Modulation
Interferons
Cell Membrane
Messenger RNA
Therapeutics
In Vitro Techniques

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Class I major histocompatibility complex enhancement by recombinant leukocyte interferon in the peripheral blood mononuclear cells and plasma of melanoma patients. / Giacomini, Patrizio; Fraioli, Rocco; Calabro, Anna Maria; Filippo, Franco Di; Natali, Pier Giorgio.

In: Cancer Research, Vol. 51, No. 2, 15.01.1991, p. 652-656.

Research output: Contribution to journalArticle

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