TY - JOUR
T1 - IL-18-induced expression of intercellular adhesion molecule-1 in human monocytes
T2 - Involvement in IL-12 and IFN-γ production in PBMC
AU - Yoshida, Atsushi
AU - Kohka Takahashi, Hideo
AU - Nishibori, Masahiro
AU - Iwagaki, Hiromi
AU - Yoshino, Tadashi
AU - Morichika, Toshihiko
AU - Yokoyama, Minori
AU - Kondo, Eisaku
AU - Akagi, Tadaatsu
AU - Tanaka, Noriaki
N1 - Funding Information:
The authors thank Dr. Y. Matsuo (Hayashibara Biochemical Laboratories, Okayama) for providing PEER cells. This study was supported in part by a grant from the Japan Society for Promotion of Science (BSAR-521/0003815).
PY - 2001/6/15
Y1 - 2001/6/15
N2 - IL-18 time- and concentration-dependently upregulated the expression of intercellular adhesion molecule-1 (ICAM-1) in a monocyte population in human PBMC as determined by FACS analysis while the expression of CD11a, CD18, CD29, CD44, and CD62L in monocytes and that of ICAM-1, CD11a, CD18, CD29, CD44, and CD62L in T cells was not influenced by IL-18. IL-18 in the same concentration range stimulated the production of IL-12, TNF-α, and IFN-γ in culture of PBMC; however, IL-18-induced expression of ICAM-1 in monocytes was not inhibited by anti-IL-12, anti-TNF-α, or anti-IFN-γ Ab, suggesting the independence of the upregulating effect of IL-18 on endogenous IL-12, TNF-α, and IFN-γ production. IL-18 also induced the aggregation of PBMC, which was prevented by anti-ICAM-1 and anti-LFA-1 Abs. On the other hand, anti-ICAM-1 and anti-LFA-1 Abs inhibited IL-18-induced production of three cytokines, IL-12, IFN-γ and TNF-α, by 60 and 40%, respectively. These results strongly suggested that the IL-18-induced upregulation of ICAM-1 and the subsequent adhesive interaction through ICAM-1 on monocytes and LFA-1 on T/NK cells generate an additional stimulatory signaling as well as an efficient paracrine environment for the IL-18-initiated cytokine cascade.
AB - IL-18 time- and concentration-dependently upregulated the expression of intercellular adhesion molecule-1 (ICAM-1) in a monocyte population in human PBMC as determined by FACS analysis while the expression of CD11a, CD18, CD29, CD44, and CD62L in monocytes and that of ICAM-1, CD11a, CD18, CD29, CD44, and CD62L in T cells was not influenced by IL-18. IL-18 in the same concentration range stimulated the production of IL-12, TNF-α, and IFN-γ in culture of PBMC; however, IL-18-induced expression of ICAM-1 in monocytes was not inhibited by anti-IL-12, anti-TNF-α, or anti-IFN-γ Ab, suggesting the independence of the upregulating effect of IL-18 on endogenous IL-12, TNF-α, and IFN-γ production. IL-18 also induced the aggregation of PBMC, which was prevented by anti-ICAM-1 and anti-LFA-1 Abs. On the other hand, anti-ICAM-1 and anti-LFA-1 Abs inhibited IL-18-induced production of three cytokines, IL-12, IFN-γ and TNF-α, by 60 and 40%, respectively. These results strongly suggested that the IL-18-induced upregulation of ICAM-1 and the subsequent adhesive interaction through ICAM-1 on monocytes and LFA-1 on T/NK cells generate an additional stimulatory signaling as well as an efficient paracrine environment for the IL-18-initiated cytokine cascade.
KW - Human
KW - ICAM-1
KW - IFN-γ
KW - IL-12
KW - IL-18
KW - LFA-1
KW - Monocytes
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U2 - 10.1006/cimm.2001.1811
DO - 10.1006/cimm.2001.1811
M3 - Article
C2 - 11520077
AN - SCOPUS:17944362580
VL - 210
SP - 106
EP - 115
JO - Cellular Immunology
JF - Cellular Immunology
SN - 0008-8749
IS - 2
ER -