Abstract |
A critical event in the pathogenesis of experimental autoimmune thyroiditis (EAT) is the entry of thyroid-specific T lymphocytes into the thyroid gland. To investigate the role of soluble mediators in that infiltration, we have assayed the expression of various chemokines in diseased thyroid glands and in cytokine-treated cultures of normal thyroid epithelial cells. MCP-1 ( monocyte chemotactic protein-1) and RANTES are produced during EAT and induced in vitro by IFN-gamma, IL-10, TNF-alpha, and IL-1beta. In vitro chemotaxis experiments using immune lymph node (LN) cells showed that RANTES attracted mTg-specific responder LN cells, whereas MCP-1 attracted mTg-specific CD4(+), CD25(+) regulator cells that secreted IL-10. The in vivo transfer of LN T cells attracted in vitro either by RANTES or by MCP-1 confirmed their opposite effects on the course of EAT.
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Authors | Claire Goulvestre, Frédéric Batteux, Jeannine Charreire |
Journal | European journal of immunology
(Eur J Immunol)
Vol. 32
Issue 12
Pg. 3435-42
(Dec 2002)
ISSN: 0014-2980 [Print] Germany |
PMID | 12432574
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Chemokine CCL2
- Chemokine CCL5
- Chemokines
- Interleukin-1
- Receptors, Interleukin-2
- Recombinant Proteins
- Tumor Necrosis Factor-alpha
- Interleukin-10
- Interferon-gamma
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Topics |
- Adoptive Transfer
- Animals
- Autoimmunity
- CD4-Positive T-Lymphocytes
(immunology)
- Cells, Cultured
- Chemokine CCL2
(biosynthesis)
- Chemokine CCL5
(biosynthesis)
- Chemokines
(biosynthesis, genetics)
- Chemotaxis
- Epithelial Cells
(drug effects, immunology)
- Female
- In Vitro Techniques
- Interferon-gamma
(pharmacology)
- Interleukin-1
(pharmacology)
- Interleukin-10
(biosynthesis, pharmacology)
- Mice
- Mice, Inbred C57BL
- Mice, Inbred CBA
- Receptors, Interleukin-2
(metabolism)
- Recombinant Proteins
- T-Lymphocyte Subsets
(immunology)
- T-Lymphocytes
(immunology)
- Thyroid Gland
(drug effects, immunology)
- Thyroiditis, Autoimmune
(etiology, genetics, immunology)
- Tumor Necrosis Factor-alpha
(pharmacology)
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