Co-expression of CD30 ligand and interleukin 4 (IL-4) receptors by acute myeloid leukaemia blasts is associated with the expansion of IL-4-producing CD30+ normal T cells

Francesca Maria Rossi, Massimo Degan, Francesca Tassan Mazzocco, Raffaele Di Francia, Donatella Aldinucci, Dalisa Poletto, Edo Vellenga, Antonio Pinto, Valter Gattei

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

CD30 ligand (CD30L), but not its cognate receptor CD30, is frequently expressed on acute myeloid leukaemia (AML) blasts. In the present study, we found that leukaemic blasts presenting surface CD30L displayed a characteristic cytokine-receptor pattern that makes them ideal targets for those cytokines usually produced by Th2-type cell subsets. In particular, even though a broad distribution of Th2 cytokine receptors by AML blasts was shown, we demonstrated the almost exclusive expression of interleukin 4 (IL-4) receptor (R), in the absence of its cognate cytokine, by CD30L+ AML. Furthermore, a number of Th2-associated markers, including CD30, IL-4 and GATA-3, were expressed by residual T cells derived from CD30L+ AML but not from CD30L- AML, in which the presence of the Th1-associated marker LAG-3 was documented in some cases. The production of IL-4 in the absence of interferon γ (IFN-γ) was also detected in CD3+/CD30+ T cells from CD30L+ AML. These results, along with the shift toward IL-4-producing specific T-cell clones observed in CD30L+ AML samples by enzyme-linked Immunospot (ELISpot) assay, were consistent with the hypothesis of a Th2 polarization taking place in T cells from CD30L+ AML. The notion that IL-4 was able to enhance in vitro proliferation of CD30L+/IL-4R+ purified leukaemic blasts suggests that the selective interaction of IL-4-producing CD30+ T cells with CD30L+ leukaemic progenitors may have a role in the progression of this particular AML subset.

Original languageEnglish
Pages (from-to)59-69
Number of pages11
JournalBritish Journal of Haematology
Volume117
Issue number1
DOIs
Publication statusPublished - 2002

Fingerprint

CD30 Ligand
Interleukin-4 Receptors
Acute Myeloid Leukemia
Interleukin-4
T-Lymphocytes
Cytokine Receptors
Cytokines
Enzyme-Linked Immunospot Assay
Th2 Cells
Interferons

Keywords

  • Acute myeloid leukaemia
  • CD30
  • CD30 ligand
  • Interleukin-4
  • Th2 T cells

ASJC Scopus subject areas

  • Hematology

Cite this

Co-expression of CD30 ligand and interleukin 4 (IL-4) receptors by acute myeloid leukaemia blasts is associated with the expansion of IL-4-producing CD30+ normal T cells. / Rossi, Francesca Maria; Degan, Massimo; Mazzocco, Francesca Tassan; Di Francia, Raffaele; Aldinucci, Donatella; Poletto, Dalisa; Vellenga, Edo; Pinto, Antonio; Gattei, Valter.

In: British Journal of Haematology, Vol. 117, No. 1, 2002, p. 59-69.

Research output: Contribution to journalArticle

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abstract = "CD30 ligand (CD30L), but not its cognate receptor CD30, is frequently expressed on acute myeloid leukaemia (AML) blasts. In the present study, we found that leukaemic blasts presenting surface CD30L displayed a characteristic cytokine-receptor pattern that makes them ideal targets for those cytokines usually produced by Th2-type cell subsets. In particular, even though a broad distribution of Th2 cytokine receptors by AML blasts was shown, we demonstrated the almost exclusive expression of interleukin 4 (IL-4) receptor (R), in the absence of its cognate cytokine, by CD30L+ AML. Furthermore, a number of Th2-associated markers, including CD30, IL-4 and GATA-3, were expressed by residual T cells derived from CD30L+ AML but not from CD30L- AML, in which the presence of the Th1-associated marker LAG-3 was documented in some cases. The production of IL-4 in the absence of interferon γ (IFN-γ) was also detected in CD3+/CD30+ T cells from CD30L+ AML. These results, along with the shift toward IL-4-producing specific T-cell clones observed in CD30L+ AML samples by enzyme-linked Immunospot (ELISpot) assay, were consistent with the hypothesis of a Th2 polarization taking place in T cells from CD30L+ AML. The notion that IL-4 was able to enhance in vitro proliferation of CD30L+/IL-4R+ purified leukaemic blasts suggests that the selective interaction of IL-4-producing CD30+ T cells with CD30L+ leukaemic progenitors may have a role in the progression of this particular AML subset.",
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T1 - Co-expression of CD30 ligand and interleukin 4 (IL-4) receptors by acute myeloid leukaemia blasts is associated with the expansion of IL-4-producing CD30+ normal T cells

AU - Rossi, Francesca Maria

AU - Degan, Massimo

AU - Mazzocco, Francesca Tassan

AU - Di Francia, Raffaele

AU - Aldinucci, Donatella

AU - Poletto, Dalisa

AU - Vellenga, Edo

AU - Pinto, Antonio

AU - Gattei, Valter

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AB - CD30 ligand (CD30L), but not its cognate receptor CD30, is frequently expressed on acute myeloid leukaemia (AML) blasts. In the present study, we found that leukaemic blasts presenting surface CD30L displayed a characteristic cytokine-receptor pattern that makes them ideal targets for those cytokines usually produced by Th2-type cell subsets. In particular, even though a broad distribution of Th2 cytokine receptors by AML blasts was shown, we demonstrated the almost exclusive expression of interleukin 4 (IL-4) receptor (R), in the absence of its cognate cytokine, by CD30L+ AML. Furthermore, a number of Th2-associated markers, including CD30, IL-4 and GATA-3, were expressed by residual T cells derived from CD30L+ AML but not from CD30L- AML, in which the presence of the Th1-associated marker LAG-3 was documented in some cases. The production of IL-4 in the absence of interferon γ (IFN-γ) was also detected in CD3+/CD30+ T cells from CD30L+ AML. These results, along with the shift toward IL-4-producing specific T-cell clones observed in CD30L+ AML samples by enzyme-linked Immunospot (ELISpot) assay, were consistent with the hypothesis of a Th2 polarization taking place in T cells from CD30L+ AML. The notion that IL-4 was able to enhance in vitro proliferation of CD30L+/IL-4R+ purified leukaemic blasts suggests that the selective interaction of IL-4-producing CD30+ T cells with CD30L+ leukaemic progenitors may have a role in the progression of this particular AML subset.

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