Dexamethasone and IL-10 stimulate glucocorticoid-induced leucine zipper synthesis by human mast cells

V. Godot, G. Garcia, F. Capel, M. Arock, I. Durand-Gasselin, Marie-Liesse Labat, D. Emilie, M. Humbert

Research output: Contribution to journalArticle

33 Citations (Scopus)

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 languageEnglish (US)
Pages (from-to)886-890
Number of pages5
JournalAllergy: European Journal of Allergy and Clinical Immunology
Volume61
Issue number7
DOIs
StatePublished - Jul 1 2006
Externally publishedYes

Fingerprint

Leucine Zippers
Mast Cells
Interleukin-10
Dexamethasone
Glucocorticoids
Interleukin-5
Interleukin-4
Histamine
Immunosuppressive Agents
Fetal Blood
Anti-Inflammatory Agents
Activator Appliances

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 journalArticle

Godot, V. ; Garcia, G. ; Capel, F. ; Arock, M. ; Durand-Gasselin, I. ; Labat, Marie-Liesse ; Emilie, D. ; Humbert, M. / Dexamethasone and IL-10 stimulate glucocorticoid-induced leucine zipper synthesis by human mast cells. In: Allergy: European Journal of Allergy and Clinical Immunology. 2006 ; Vol. 61, No. 7. pp. 886-890.
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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.

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