REVIEW - Immune mechanisms in thyroid eye disease

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Thyroid. 2008 Sep;18(9):959-65.

Immune mechanisms in thyroid eye disease.

Lehmann GM, Feldon SE, TJ, Phipps RP.

Department of Environmental Medicine, University of Rochester,

Rochester, New York 14642, USA.

Thyroid eye disease (TED) is an inflammatory condition of the orbit

closely associated with Graves' disease. During the course of TED,

fibrosis can develop around the extraocular muscles, and excess

extracellular matrix and fat accumulates in the periorbital space.

This dramatic remodeling results in protrusion of the eye, also known

as exophthalmos. Current treatments are sometimes effective in

alleviating the symptoms of the disease, but there remains a demand

for treatments that prevent or reverse the pathological alterations of

orbital tissues. Such treatments may become available as a result of

research aimed at understanding the mechanism by which Graves' disease

leads to specific remodeling of orbital tissues. Recent findings have

uncovered the importance of intercellular communication between

autoreactive T cells and orbital fibroblasts. When orbital fibroblasts

are activated, possibly by Graves' disease-related autoantibodies,

they release T cell chemoattractants, initiating an interaction in

which these cells activate each other. These interactions ultimately

result in fibroblasts expressing extracellular matrix molecules,

proliferating and differentiating into myofibroblasts or

lipofibroblasts. Although the mechanisms underlying these processes

are not completely understood, several currently available therapeutic

strategies might interrupt the signaling between B and T cells and

fibroblasts, thereby treating the clinical manifestations of TED.

PMID: 18752427

http://www.ncbi.nlm.nih.gov/pubmed/18752427

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