Abstract
Background: Glucocorticoids (GCs) decrease tissue mast cell (MC) number and prevent their activation via their high-affinity IgE receptor. Glucocorticoid-induced leucine zipper (GILZ) is one of the GC-induced genes, which inhibits the functions of the transcriptional activators AP-1 and NF-κB. GILZ appears to be a critical actor in the anti-inflammatory and immunosuppressive effects of GCs in human T lymphocytes, macrophages and dendritic cells. Aims of the study: We investigated whether GILZ was produced by human MCs and whether GILZ synthesis was stimulated by GCs. We also investigated whether GILZ production was modulated by (i) IL-10, because of its common immunosuppressive properties with GCs, (ii) histamine because of its pro-inflammatory properties and (iii) IL-4 and IL-5 because of their ability to favour MC survival and proliferation with SCF. Methods: The human MC lines HMC-1 5C6 and LAD-2, and cord blood-derived MCs (CB-MCs) were cultured alone or in the presence of GCs, IL-10, histamine, IL-4 or IL-5. The expression of GILZ was evaluated by using RT-PCR, Western blotting or immunocytochemistry. Results: We found that human MC lines and CB-MCs constitutively produce GILZ. We also show that GCs and IL-10 stimulate GILZ production by human MCs. Our present results indicate that histamine, IL-4 and IL-5 alone or in combination with SCF do not downregulate GILZ production by MCs. Conclusions: These results show that GCs and IL-10 stimulate GILZ production by human MCs. As GILZ mediates anti-inflammatory effects of GCs in immune cells, we speculate that GILZ could account for the deactivation of MCs by GCs and IL-10.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 886-890 |
| Number of pages | 5 |
| Journal | Allergy: European Journal of Allergy and Clinical Immunology |
| Volume | 61 |
| Issue number | 7 |
| DOIs | |
| State | Published - Jul 1 2006 |
| Externally published | Yes |
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Keywords
- GILZ
- Glucocorticoids
- IL-10
- Mast cells
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
Cite this
Dexamethasone and IL-10 stimulate glucocorticoid-induced leucine zipper synthesis by human mast cells. / Godot, V.; Garcia, G.; Capel, F.; Arock, M.; Durand-Gasselin, I.; Labat, Marie-Liesse; Emilie, D.; Humbert, M.
In: Allergy: European Journal of Allergy and Clinical Immunology, Vol. 61, No. 7, 01.07.2006, p. 886-890.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Dexamethasone and IL-10 stimulate glucocorticoid-induced leucine zipper synthesis by human mast cells
AU - Godot, V.
AU - Garcia, G.
AU - Capel, F.
AU - Arock, M.
AU - Durand-Gasselin, I.
AU - Labat, Marie-Liesse
AU - Emilie, D.
AU - Humbert, M.
PY - 2006/7/1
Y1 - 2006/7/1
N2 - Background: Glucocorticoids (GCs) decrease tissue mast cell (MC) number and prevent their activation via their high-affinity IgE receptor. Glucocorticoid-induced leucine zipper (GILZ) is one of the GC-induced genes, which inhibits the functions of the transcriptional activators AP-1 and NF-κB. GILZ appears to be a critical actor in the anti-inflammatory and immunosuppressive effects of GCs in human T lymphocytes, macrophages and dendritic cells. Aims of the study: We investigated whether GILZ was produced by human MCs and whether GILZ synthesis was stimulated by GCs. We also investigated whether GILZ production was modulated by (i) IL-10, because of its common immunosuppressive properties with GCs, (ii) histamine because of its pro-inflammatory properties and (iii) IL-4 and IL-5 because of their ability to favour MC survival and proliferation with SCF. Methods: The human MC lines HMC-1 5C6 and LAD-2, and cord blood-derived MCs (CB-MCs) were cultured alone or in the presence of GCs, IL-10, histamine, IL-4 or IL-5. The expression of GILZ was evaluated by using RT-PCR, Western blotting or immunocytochemistry. Results: We found that human MC lines and CB-MCs constitutively produce GILZ. We also show that GCs and IL-10 stimulate GILZ production by human MCs. Our present results indicate that histamine, IL-4 and IL-5 alone or in combination with SCF do not downregulate GILZ production by MCs. Conclusions: These results show that GCs and IL-10 stimulate GILZ production by human MCs. As GILZ mediates anti-inflammatory effects of GCs in immune cells, we speculate that GILZ could account for the deactivation of MCs by GCs and IL-10.
AB - Background: Glucocorticoids (GCs) decrease tissue mast cell (MC) number and prevent their activation via their high-affinity IgE receptor. Glucocorticoid-induced leucine zipper (GILZ) is one of the GC-induced genes, which inhibits the functions of the transcriptional activators AP-1 and NF-κB. GILZ appears to be a critical actor in the anti-inflammatory and immunosuppressive effects of GCs in human T lymphocytes, macrophages and dendritic cells. Aims of the study: We investigated whether GILZ was produced by human MCs and whether GILZ synthesis was stimulated by GCs. We also investigated whether GILZ production was modulated by (i) IL-10, because of its common immunosuppressive properties with GCs, (ii) histamine because of its pro-inflammatory properties and (iii) IL-4 and IL-5 because of their ability to favour MC survival and proliferation with SCF. Methods: The human MC lines HMC-1 5C6 and LAD-2, and cord blood-derived MCs (CB-MCs) were cultured alone or in the presence of GCs, IL-10, histamine, IL-4 or IL-5. The expression of GILZ was evaluated by using RT-PCR, Western blotting or immunocytochemistry. Results: We found that human MC lines and CB-MCs constitutively produce GILZ. We also show that GCs and IL-10 stimulate GILZ production by human MCs. Our present results indicate that histamine, IL-4 and IL-5 alone or in combination with SCF do not downregulate GILZ production by MCs. Conclusions: These results show that GCs and IL-10 stimulate GILZ production by human MCs. As GILZ mediates anti-inflammatory effects of GCs in immune cells, we speculate that GILZ could account for the deactivation of MCs by GCs and IL-10.
KW - GILZ
KW - Glucocorticoids
KW - IL-10
KW - Mast cells
UR - http://www.scopus.com/inward/record.url?scp=33745164851&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33745164851&partnerID=8YFLogxK
U2 - 10.1111/j.1398-9995.2006.01065.x
DO - 10.1111/j.1398-9995.2006.01065.x
M3 - Article
VL - 61
SP - 886
EP - 890
JO - Allergy: European Journal of Allergy and Clinical Immunology
JF - Allergy: European Journal of Allergy and Clinical Immunology
SN - 0108-1675
IS - 7
ER -