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J. Biol. Chem., Vol. 265, Issue 36, 22499-22505, 12, 1990
MK Spriggs, PJ Lioubin, J Slack, SK Dower, U Jonas, D Cosman, JE Sims and J Bauer
Primary human monocytes and the human monocytic cell line THP-1 were
induced to express receptors for interleukin-1 alpha (IL-1 alpha) and IL-1
beta. Treatment of primary monocytes with dexamethasone resulted in a
10-fold increase in receptor number over untreated cells, to approximately
2,000 receptors/cell. Treatment of THP-1 cells with phorbol ester followed
by prostaglandin E2 and dexamethasone resulted in the expression of
approximately 30,000 receptors/cell. Competitive binding assays on THP-1
cells showed that both IL-1 alpha and IL-1 beta bind to the same receptor.
The monocyte IL-1R is significantly smaller (63 kDa) than the T cell IL-1R
(80 kDa) and is immunologically distinct. However, induction of monocytes
and monocytic cell lines leads to the appearance of an abundant mRNA of
approximately 5,000 bases which hybridizes to a cDNA probe from the T
cell-type IL-1R. Sequence data obtained from a cDNA clone of this mRNA
indicate that the message is identical to the T cell IL-1R mRNA throughout
the coding region. A smaller mRNA, also homologous to the T cell IL-1R
mRNA, accumulated in induced THP-1 cells and has a shorter 3'-untranslated
region than the larger. Data are presented which suggest that neither form
of this message encodes the 63-kDa IL-1R, but rather that this protein is
the product of a separate nonhomologous mRNA.
Induction of an interleukin-1 receptor (IL-1R) on monocytic cells. Evidence that the receptor is not encoded by a T cell-type IL-1R mRNA
Immunex Research and Development Corporation, Seattle, Washington 98101.
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