1992
DOI: 10.1182/blood.v79.9.2356.bloodjournal7992356
|View full text |Cite
|
Sign up to set email alerts
|

Effect of interleukin-1 (IL-1) blockade on cytokine synthesis: I. IL-1 receptor antagonist inhibits IL-1-induced cytokine synthesis and blocks the binding of IL-1 to its type II receptor on human monocytes

Abstract: Interleukin-1 (IL-1) induces IL-1, tumor necrosis factor alpha (TNF alpha), and IL-6 gene expression and synthesis in a variety of cells. In this study, we investigated the ability of human recombinant IL-1 receptor antagonist (IL-1ra) to inhibit IL-1-induced cytokine production in human peripheral blood mononuclear cells (PBMC) and isolated monocytes. IL-1ra alone at concentrations as high as 1 microgram/mL did not induce IL-1 alpha, IL-1 beta, TNF alpha, or IL-6 synthesis. Suppression of IL-1-induced IL-1, T… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1
1

Citation Types

4
15
0

Year Published

1992
1992
2008
2008

Publication Types

Select...
6
1

Relationship

0
7

Authors

Journals

citations
Cited by 15 publications
(19 citation statements)
references
References 0 publications
4
15
0
Order By: Relevance
“…Likewise, a 100-fold molar excess of IL-IRa is needed to block the fever induced by a bolus injection of IL-1 in rabbits . This is consistent with the concentration of IL-IRa needed to block IL-1 activity in cultured cells (Arend et al 1990, Granowitz et al 1992a).…”
Section: A Effects Of Il-lra In Animalssupporting
confidence: 80%
“…Likewise, a 100-fold molar excess of IL-IRa is needed to block the fever induced by a bolus injection of IL-1 in rabbits . This is consistent with the concentration of IL-IRa needed to block IL-1 activity in cultured cells (Arend et al 1990, Granowitz et al 1992a).…”
Section: A Effects Of Il-lra In Animalssupporting
confidence: 80%
“…As reported previously, LPS induced a marked stimulation of G-CSF release in PBMC [7,8,16]. LPS also significantly induced IL-1, which has previously been shown to induce G-CSF production [7].…”
Section: Discussionsupporting
confidence: 66%
“…An explanation for the lack of effect of endogenous IL-1 on G-CSF production, even though the former is produced in large amounts, might be the simultaneous induction of large amounts of IL-1ra, a natural antagonist to IL-1. In vitro, IL-1ra acts as a direct antagonist to IL-1 in that it inhibits the binding of IL-1 to IL-1 receptors Type I and II (IL-1 Rt I/II) [16], and thereby suppresses IL-1 function. The quantities of IL-1ra produced might, by themselves, suffice to block all the endogenously produced IL-1 and thus may inhibit a potential stimulatory effect of endogenous IL-1 on G-CSF production.…”
Section: Discussionmentioning
confidence: 99%
“…Thus, IL-1RA reduces the cytokine and proliferative response of T cells to mitogens 20,21 and the cytokine secretion of inflammatory cells after IL-1 and endotoxin stimulation. 18,19 Clinical efficiency of IL-1RA has been indicated in patients with rheumatoid arthritis and GVHD. 22 From the evidence for this immunosuppressive capacity of IL-1RA, it could be hypothesized that the escalating amounts of WBC-derived free IL-1RA in supernatants of non-WBC-reduced stored blood components contribute to the immunosuppressive effect of blood transfusion.…”
Section: Discussionmentioning
confidence: 99%
“…Because of its marked anti-inflammatory and immunosuppressive capacity, [18][19][20][21][22] IL-1RA could be involved in transfusion-associated immunosuppression. Therefore, we decided to investigate the kinetics and mechanisms of IL-1RA release in both C-RBCs and F-RBCs using a prospectively approved study design.…”
Section: Increase In Il-1ra Level Correlates With Loss Of Wbcs In C-rbcsmentioning
confidence: 99%