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10.1038/nrendo.2014.226

http://scihub22266oqcxt.onion/10.1038/nrendo.2014.226
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C4687015!4687015!25560705
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suck abstract from ncbi


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pmid25560705      Nat+Rev+Endocrinol 2015 ; 11 (3): 171-81
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  • Recognizing the Putative Role for TSH Receptor Expressing Fibrocytes in Thyroid-Associated Ophthalmopathy may solve several mysteries #MMPMID25560705
  • Smith TJ
  • Nat Rev Endocrinol 2015[Mar]; 11 (3): 171-81 PMID25560705show ga
  • Thyroid-associated ophthalmopathy (TAO) remains the vexing and undertreated ocular component of Graves? disease where orbital tissues undergo extensive remodeling. We have recently introduced the concept that CD34+ fibrocytes, bone marrow derived monocyte lineage precursor cells express the thyrotropin receptor (TSHR) and several other proteins traditionally thought to be expressed uniquely in the thyroid. TSHR-engaged fibrocytes generate extremely high levels of several inflammatory cytokines. Acting in concert with TSHR, the insulin-like growth factor 1 receptor (IGF-1R) expressed by fibrocytes appears to be necessary for TSHR-dependent cytokine production since anti-IGF-1R blocking antibodies attenuate these actions of TSH. Further, circulating fibrocytes become more abundant and appear to infiltrate orbital connective tissues in TAO where they may transition to CD34+ fibroblasts. We currently postulate that the infiltration of fibrocytes into the orbit and their unique biosynthetic repertoire and proinflammatory/profibrotic phenotype account for the characteristic properties exhibited by orbital connective tissues that render them susceptible to TAO. Further, it may be possible to utilize these very recent insights to therapeutically target pathogenic orbital fibrocytes selectively utilizing recently developed biologic agents which interfere with TSHR and IGF-1R signaling.
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