Abstract
The activation of T cells plays a role in antitumor response. Monocytes activate T cells by inducing the cell-to-cell interaction that involves the engagement of adhesion molecules with their ligands, and the production of IL-18. The authors examined the effect of the quinazoline-based α1-adrenergic receptor antagonists bunazosin, doxazosin, prazosin, and terazosin on the expression of adhesion molecules such as ICAM-1, B7.1, B7.2, CD40, and CD40L on monocytes isolated from human peripheral blood mononuclear cells. Doxazosin, prazosin, and terazosin induced the expression of ICAM-1 and CD40 but had no effect on the expression of B7.1, B7.2, and CD40L. Moreover, IL-18 was detected in the medium of incubated monocytes treated with doxazosin, prazosin, and terazosin. Bunazosin did not affect adhesion molecule expression and IL-18 production, suggesting that the chemical structure of quinazoline might not be related to the effect of doxazosin, prazosin, and terazosin. Although caspase-1 inhibitor completely abolished the production of IL-18, anti-IL-18 mAb and caspase-1 inhibitor partially inhibited the increase in ICAM-1 and CD40 expression induced by doxazosin, prazosin, and terazosin. Doxazosin, prazosin, and terazosin can induce monocyte activation with a specific pattern of expression of adhesion molecules and IL-18 production, and this may lead to T-cell activation through the cell-to-cell interaction. The activation of T cells induced by the increase of the expression of ICAM-1 and CD40 and the production of IL-18 may be involved in the anti-cancer effects of doxazosin, prazosin, and terazosin.
| Original language | English |
|---|---|
| Pages (from-to) | 40-43 |
| Number of pages | 4 |
| Journal | Journal of Immunotherapy |
| Volume | 28 |
| Issue number | 1 |
| Publication status | Published - Jan 2005 |
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Keywords
- α1-antagonists
- CD40
- ICAM-1
- IL-18
- Monocytes
ASJC Scopus subject areas
- Cancer Research
- Pharmacology
- Immunology
Cite this
α1-adrenergic receptor antagonists induce production of IL-18 and expression of ICAM-1 and CD40 in human monocytes. / Takahashi, Hideo Kohka; Iwagaki, Hiromi; Tamura, Ryuji; Katsuno, Goutarou; Xue, Dong; Sugita, Sachi; Mori, Shuji; Yoshino, Tadashi; Tanaka, Noriaki; Nishibori, Masahiro.
In: Journal of Immunotherapy, Vol. 28, No. 1, 01.2005, p. 40-43.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - α1-adrenergic receptor antagonists induce production of IL-18 and expression of ICAM-1 and CD40 in human monocytes
AU - Takahashi, Hideo Kohka
AU - Iwagaki, Hiromi
AU - Tamura, Ryuji
AU - Katsuno, Goutarou
AU - Xue, Dong
AU - Sugita, Sachi
AU - Mori, Shuji
AU - Yoshino, Tadashi
AU - Tanaka, Noriaki
AU - Nishibori, Masahiro
PY - 2005/1
Y1 - 2005/1
N2 - The activation of T cells plays a role in antitumor response. Monocytes activate T cells by inducing the cell-to-cell interaction that involves the engagement of adhesion molecules with their ligands, and the production of IL-18. The authors examined the effect of the quinazoline-based α1-adrenergic receptor antagonists bunazosin, doxazosin, prazosin, and terazosin on the expression of adhesion molecules such as ICAM-1, B7.1, B7.2, CD40, and CD40L on monocytes isolated from human peripheral blood mononuclear cells. Doxazosin, prazosin, and terazosin induced the expression of ICAM-1 and CD40 but had no effect on the expression of B7.1, B7.2, and CD40L. Moreover, IL-18 was detected in the medium of incubated monocytes treated with doxazosin, prazosin, and terazosin. Bunazosin did not affect adhesion molecule expression and IL-18 production, suggesting that the chemical structure of quinazoline might not be related to the effect of doxazosin, prazosin, and terazosin. Although caspase-1 inhibitor completely abolished the production of IL-18, anti-IL-18 mAb and caspase-1 inhibitor partially inhibited the increase in ICAM-1 and CD40 expression induced by doxazosin, prazosin, and terazosin. Doxazosin, prazosin, and terazosin can induce monocyte activation with a specific pattern of expression of adhesion molecules and IL-18 production, and this may lead to T-cell activation through the cell-to-cell interaction. The activation of T cells induced by the increase of the expression of ICAM-1 and CD40 and the production of IL-18 may be involved in the anti-cancer effects of doxazosin, prazosin, and terazosin.
AB - The activation of T cells plays a role in antitumor response. Monocytes activate T cells by inducing the cell-to-cell interaction that involves the engagement of adhesion molecules with their ligands, and the production of IL-18. The authors examined the effect of the quinazoline-based α1-adrenergic receptor antagonists bunazosin, doxazosin, prazosin, and terazosin on the expression of adhesion molecules such as ICAM-1, B7.1, B7.2, CD40, and CD40L on monocytes isolated from human peripheral blood mononuclear cells. Doxazosin, prazosin, and terazosin induced the expression of ICAM-1 and CD40 but had no effect on the expression of B7.1, B7.2, and CD40L. Moreover, IL-18 was detected in the medium of incubated monocytes treated with doxazosin, prazosin, and terazosin. Bunazosin did not affect adhesion molecule expression and IL-18 production, suggesting that the chemical structure of quinazoline might not be related to the effect of doxazosin, prazosin, and terazosin. Although caspase-1 inhibitor completely abolished the production of IL-18, anti-IL-18 mAb and caspase-1 inhibitor partially inhibited the increase in ICAM-1 and CD40 expression induced by doxazosin, prazosin, and terazosin. Doxazosin, prazosin, and terazosin can induce monocyte activation with a specific pattern of expression of adhesion molecules and IL-18 production, and this may lead to T-cell activation through the cell-to-cell interaction. The activation of T cells induced by the increase of the expression of ICAM-1 and CD40 and the production of IL-18 may be involved in the anti-cancer effects of doxazosin, prazosin, and terazosin.
KW - α1-antagonists
KW - CD40
KW - ICAM-1
KW - IL-18
KW - Monocytes
UR - http://www.scopus.com/inward/record.url?scp=19944428889&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=19944428889&partnerID=8YFLogxK
M3 - Article
C2 - 15614043
AN - SCOPUS:19944428889
VL - 28
SP - 40
EP - 43
JO - Journal of Immunotherapy
JF - Journal of Immunotherapy
SN - 1524-9557
IS - 1
ER -