Production and secretion of interleukin 1 receptor antagonist in monocytes and keratinocytes

A. Corradi, A. Bajetto, F. Cozzolino, A. Rubartelli

Research output: Contribution to journalArticle

Abstract

IL-1 receptor antagonist (IL-1ra) is a newly described member of the IL-1 family, isolated from supernatants of Ig stimulated monocytes, that binds competitively to IL-1 receptors without stimulating target cells (1-3). Also epithelial cells produce IL-1ra in a form which lacks a secretory signal sequence (4). Here we have compared the biosynthesis and secretion of IL-1ra in monocytes and keratinocytes. Our data show that monocytes produce two molecular forms of IL-1ra, of 18 Kd and 23 Kd respectively, which differ in the degree of glycosylation. Both forms are secreted via the "classical" endoplasmic reticulum (ER)-Golgi secretory pathway. By contrast keratinocytes produce IL-1ra in a molecular form of 20 Kd, which is not N-glycosylated: 20 Kd IL-1ra is detectable in supernatants of keratinocytes, although in small amounts. The presence of IL-1ra in keratinocytes cultures fluids is not inhibited by Brefeldin A (BFA), suggesting a possible secretion through the leaderless secretory pathway.

Original languageEnglish
JournalCytotechnology
Volume11
Issue number1 Supplement
DOIs
Publication statusPublished - Jan 1993

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Interleukin-1 Receptors
Keratinocytes
Monocytes
Glycosylation
Secretory Pathway
Biosynthesis
Brefeldin A
Fluids
Protein Sorting Signals
Interleukin-1
Endoplasmic Reticulum
Epithelial Cells

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology
  • Biotechnology

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Production and secretion of interleukin 1 receptor antagonist in monocytes and keratinocytes. / Corradi, A.; Bajetto, A.; Cozzolino, F.; Rubartelli, A.

In: Cytotechnology, Vol. 11, No. 1 Supplement, 01.1993.

Research output: Contribution to journalArticle

Corradi, A. ; Bajetto, A. ; Cozzolino, F. ; Rubartelli, A. / Production and secretion of interleukin 1 receptor antagonist in monocytes and keratinocytes. In: Cytotechnology. 1993 ; Vol. 11, No. 1 Supplement.
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