Synergistic activation of granulocyte-macrophage colony-stimulating factor production by IL-1 and IL-2 in murine Th1 cells

H. Quill, A. Gaur, Deborah M Brown, A. J. Infante, R. P. Phipps

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Abstract

Recent reports indicate that murine CD4 + Th1-type cloned T cells are insensitive to IL-1 because specific IL-1R are not detected on these cells and IL-1 does not modulate proliferative responses. However, we have determined that Th1 clones can respond to IL-1, because they function synergistically with IL-2 to induce granulocyte-macrophage-CSF secretion. This response to IL-1 plus IL-2 could be induced by IL-1α or IL-1β and by membrane-bound IL-1 on macrophages. However, IL-1R could not be detected, and Th1 cells did not respond to IL-4 in the presence or absence of IL-1, as measured by either proliferation or granulocyte-macrophage-CSF production. Therefore, IL-1 functioned as a cofactor in Th1 cells stimulated with IL-2, but not with IL-4. A possible mechanism whereby IL-1 activates Th1 cells is discussed.

Original languageEnglish (US)
Pages (from-to)2242-2247
Number of pages6
JournalJournal of Immunology
Volume143
Issue number7
StatePublished - Jan 1 1989

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Th1 Cells
Granulocyte-Macrophage Colony-Stimulating Factor
Interleukin-1
Interleukin-2
Macrophages
Granulocytes
Interleukin-4
Clone Cells
T-Lymphocytes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Synergistic activation of granulocyte-macrophage colony-stimulating factor production by IL-1 and IL-2 in murine Th1 cells. / Quill, H.; Gaur, A.; Brown, Deborah M; Infante, A. J.; Phipps, R. P.

In: Journal of Immunology, Vol. 143, No. 7, 01.01.1989, p. 2242-2247.

Research output: Contribution to journalArticle

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AB - Recent reports indicate that murine CD4 + Th1-type cloned T cells are insensitive to IL-1 because specific IL-1R are not detected on these cells and IL-1 does not modulate proliferative responses. However, we have determined that Th1 clones can respond to IL-1, because they function synergistically with IL-2 to induce granulocyte-macrophage-CSF secretion. This response to IL-1 plus IL-2 could be induced by IL-1α or IL-1β and by membrane-bound IL-1 on macrophages. However, IL-1R could not be detected, and Th1 cells did not respond to IL-4 in the presence or absence of IL-1, as measured by either proliferation or granulocyte-macrophage-CSF production. Therefore, IL-1 functioned as a cofactor in Th1 cells stimulated with IL-2, but not with IL-4. A possible mechanism whereby IL-1 activates Th1 cells is discussed.

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