Exp Clin Endocrinol Diabetes 2000; Vol. 108(2): 67-71
DOI: 10.1055/s-2000-5797
Review

© Johann Ambrosius Barth

Thyrocyte-interleukin-1 interactions

Å. K. Rasmussen, K. Bendtzen, U. Feldt-Rasmussen
  • Medical Department of Endocrinology & Institute of Inflammatory Research, Rigshospitalet, Copenhagen University Hospital, Denmark
Further Information

Publication History

Publication Date:
31 December 2000 (online)

Summary:

Autoimmune thyroid disease is the most common organ-specific autoimmune disease and is a very common cause of thyroid dysfunction such as autoimmune hypothyroidism, Graves' disease and postpartum thyroiditis. The thyroid gland from patients with autoimmune thyroid disease is morphologically characterized by massive infiltration of lymphoid cells. The interleukin-1 (IL-1) family of molecules is together with other cytokines an integral component of the complex intercellular communication required to mount and control an immune response.

IL-1α/β in moderate and high concentrations reversibly inhibit thyroid cell function, while IL-1β in low concentrations stimulates thyroid cell function. The biphasic, non-cytotoxic and reversible influence of IL-1 supports a role of IL-1 in the physiological regulation of thyroid cell function. IL-1 stimulates the guanylate mediated pathways and inhibits the adenylate cyclase mediated pathways. All IL-1 effects are counteracted by IL-1 receptor antagonist indicating that the effects are exerted through activation of specific IL-1 receptors on thyrocytes. Furthermore, IL-1 induces or enhances expression of a number of immunologically active molecules such as adhesion molecules, cytokines, and complement regulatory proteins in thyroid epithelial cells. IL-1 may thus play a role during physiological as well as pathophysiological conditions contributing to for example the euthyroid sick syndrome and development of thyroid autoimmunity.

This review summarizes current litterature on the phenomenological in vitro influence of IL-1 on the thyroid cell.

Abbreviations: cAMP: cyclic adenylate monophosphate, cGMP: cyclic guanylate monophosphate, FRTL: Fischer rat thyroid line, ICAM: intercellular adhesion molecule, IL-1: interleukin-1, IL-6: interleukin-6, IL-8: interleukin-8, IL-1RA: Interleukin-1 receptor antagonist, L-NMMA: L-NG-monomethyl-arginine, NIS: Na+/I- symporter, NO: nitric oxide, rh: recombinant human, TEC: thyroid epithelial cells, Tg: thyroglobulin, TPO: thyroid peroxidase, TSH: thyrotropin

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Åse Krogh RasmussenM.D. 

Medical Department of Endocrinology PE

Rigshospitalet/National University Hospital

Blegdamsvej 9

DK-2100 Copenhagen Ø, Denmark

Phone: +45 35 45 23 99

Fax: +45 35 45 22 40

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