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GILZ expression in human dendritic cells redirects their maturation and prevents antigen-specific T lymphocyte response
- Source :
- Blood. 107(5)
- Publication Year :
- 2005
-
Abstract
- Interleukin (IL)-10 and glucocorticoids (GCs) inhibit the ability of antigen-presenting dendritic cells (DCs) to stimulate T lymphocytes. We show that induction of GILZ (GC-induced leucine zipper) is involved in this phenomenon. IL-10, dexamethasone (DEX), and transforming growth factor (TGF)β stimulate GILZ production in human immature DCs derived from monocytes and from CD34+ cells. GILZ is necessary and sufficient for DEX, IL-10, and TGFβ modulation of CD80, CD83, CD86, immunoglobulin-like transcript (ILT)-3, and B7-H1 expression by DCs, and alteration of DC functions. GILZ stimulates the production of IL-10 by immature DCs and prevents the production of inflammatory chemokines by CD40L-activated DCs. In contrast, GILZ does not prevent CD40 ligand-mediated inhibition of phagocytosis, indicating that it affects some but not all aspects of DC maturation. GILZ prevents DCs from activating antigen-specific T lymphocyte responses. Administration of GCs to patients stimulates GILZ expression in their circulating antigen-presenting cells, and this contributes to the weak lymphocyte responses of GC-treated patients. Thus, regulation of GILZ expression is an important factor determining the decision of DCs whether or not to stimulate T lymphocytes, and IL-10, GCs, and TGFβ share this mechanism for influencing DC functions and the balance between immune response and tolerance.
- Subjects :
- Chemokine
Lymphocyte
T-Lymphocytes
Immunology
Anti-Inflammatory Agents
chemical and pharmacologic phenomena
Biology
Lymphocyte Activation
Biochemistry
Immune system
Antigens, CD
medicine
Immune Tolerance
Humans
Cells, Cultured
CD86
CD40
hemic and immune systems
Cell Differentiation
Cell Biology
Hematology
T lymphocyte
Dendritic Cells
Cell biology
medicine.anatomical_structure
Gene Expression Regulation
biology.protein
Cytokines
CD80
Transforming growth factor
Transcription Factors
Subjects
Details
- ISSN :
- 00064971
- Volume :
- 107
- Issue :
- 5
- Database :
- OpenAIRE
- Journal :
- Blood
- Accession number :
- edsair.doi.dedup.....036380ad1688bfa4e014b59a0b25c7f2