Abstract
Expression of major histocompatibility complex class II molecules, Ia, can be significantly augmented by interferon-γ (IFN-γ) in macrophages. In this study we demonstrate that platelet-activating factor (PAF) was also a potent inducer of Ia antigen expression on macrophages, PAF-induced Ia expression was both time- and dose-dependent. Maximal Ia expression was induced with 25 nM PAF after 3-h exposure to PAF. Ia expression in macrophages stimulated with PAF for 24 h was not significantly greater than unstimulated macrophages. Treatment of macrophages with IFN-γ and PAF did not affect either the kinetics or concentration required for maximal Ia expression induced by either IFN-γ or PAF. PAF-induced Ia expression was inhibited by the specific PAF receptor antagonists, WEB 2086, Ro 24-0238, and Ro 24-4637, indicating a receptor-mediated event. Like IFN-γ-induced Ia expression, PAF activity was inhibited by prostaglandin E2 (PGE2). However, that expression was only inhibited after 24 h when macrophages were treated with the PGE2 synthesis inhibitors, flurbiprofen and indomethacin. These findings demonstrate that PAF, along with its role as a potent proinflammatory mediator, was also capable of inducing Ia expression on macrophages through the PAF receptor and that expression was altered by PGE2.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 845-851 |
| Number of pages | 7 |
| Journal | Journal of Leukocyte Biology |
| Volume | 62 |
| Issue number | 6 |
| State | Published - Dec 1997 |
Fingerprint
Keywords
- Class II
- Interferon- γ
- Major histocompatibility complex
- Prostaglandin E
- Receptor
ASJC Scopus subject areas
- Cell Biology
Cite this
Induction and modulation of macrophage ia antigen expression by platelet-activating factor. / Erickson, Kent L; Howard, Angela D.; Hubbard, Neil.
In: Journal of Leukocyte Biology, Vol. 62, No. 6, 12.1997, p. 845-851.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Induction and modulation of macrophage ia antigen expression by platelet-activating factor
AU - Erickson, Kent L
AU - Howard, Angela D.
AU - Hubbard, Neil
PY - 1997/12
Y1 - 1997/12
N2 - Expression of major histocompatibility complex class II molecules, Ia, can be significantly augmented by interferon-γ (IFN-γ) in macrophages. In this study we demonstrate that platelet-activating factor (PAF) was also a potent inducer of Ia antigen expression on macrophages, PAF-induced Ia expression was both time- and dose-dependent. Maximal Ia expression was induced with 25 nM PAF after 3-h exposure to PAF. Ia expression in macrophages stimulated with PAF for 24 h was not significantly greater than unstimulated macrophages. Treatment of macrophages with IFN-γ and PAF did not affect either the kinetics or concentration required for maximal Ia expression induced by either IFN-γ or PAF. PAF-induced Ia expression was inhibited by the specific PAF receptor antagonists, WEB 2086, Ro 24-0238, and Ro 24-4637, indicating a receptor-mediated event. Like IFN-γ-induced Ia expression, PAF activity was inhibited by prostaglandin E2 (PGE2). However, that expression was only inhibited after 24 h when macrophages were treated with the PGE2 synthesis inhibitors, flurbiprofen and indomethacin. These findings demonstrate that PAF, along with its role as a potent proinflammatory mediator, was also capable of inducing Ia expression on macrophages through the PAF receptor and that expression was altered by PGE2.
AB - Expression of major histocompatibility complex class II molecules, Ia, can be significantly augmented by interferon-γ (IFN-γ) in macrophages. In this study we demonstrate that platelet-activating factor (PAF) was also a potent inducer of Ia antigen expression on macrophages, PAF-induced Ia expression was both time- and dose-dependent. Maximal Ia expression was induced with 25 nM PAF after 3-h exposure to PAF. Ia expression in macrophages stimulated with PAF for 24 h was not significantly greater than unstimulated macrophages. Treatment of macrophages with IFN-γ and PAF did not affect either the kinetics or concentration required for maximal Ia expression induced by either IFN-γ or PAF. PAF-induced Ia expression was inhibited by the specific PAF receptor antagonists, WEB 2086, Ro 24-0238, and Ro 24-4637, indicating a receptor-mediated event. Like IFN-γ-induced Ia expression, PAF activity was inhibited by prostaglandin E2 (PGE2). However, that expression was only inhibited after 24 h when macrophages were treated with the PGE2 synthesis inhibitors, flurbiprofen and indomethacin. These findings demonstrate that PAF, along with its role as a potent proinflammatory mediator, was also capable of inducing Ia expression on macrophages through the PAF receptor and that expression was altered by PGE2.
KW - Class II
KW - Interferon- γ
KW - Major histocompatibility complex
KW - Prostaglandin E
KW - Receptor
UR - http://www.scopus.com/inward/record.url?scp=0031456721&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0031456721&partnerID=8YFLogxK
M3 - Article
C2 - 9400826
AN - SCOPUS:0031456721
VL - 62
SP - 845
EP - 851
JO - Journal of Leukocyte Biology
JF - Journal of Leukocyte Biology
SN - 0741-5400
IS - 6
ER -