Narration on the pathophysiology of thyroid eye disease.
English (North American)
Middle Aged (35-54)
North American, US General American (GenAm), US West Coast (California, Portland)
Note: Transcripts are generated using speech recognition software and may contain errors.
thyroid eye disease or TD. Is a serious progressive and vision threatening autoimmune disease emerging research demonstrates that the orbital fibroblast, a specialized cell responsible for tissue repair is central to the path of physiology of T. E. D. Pathogenic orbital fibroblasts are believed to recruit fiber sites and lymphocytes that infiltrate the orbit fiber sites differentiate into orbital fibroblasts which enhance t cell proliferation and activation T cells and B cells activate orbital fibroblasts and secrete cytokines and insulin like growth factor one receptor or IGF one R. And thyroid stimulating hormone receptor. Or TSH are auto antibodies which contribute to the inflammatory cascade to co localized receptors reside on the surface of orbital fibroblasts. The TSH are the I. G. F. One R. A gatekeeper of orbital fibroblast activation and potentially ation of effects. Auto antibodies activate I G. F. One R. And T. S. H. R. And Crosstalk mediated by beta arrest and creates a receptor signaling complex that stimulates orbital fibroblasts. Once activated orbital fibroblasts proliferate and produce inflammatory cytokines and the hydra filic highly Iran in which enlarges orbital tissue volume activated orbital fibroblasts differentiate into a deep insights and myo fibroblasts which contribute respectively to add up a genesis and fibrosis of the orbital tissues. The ensuing tissue expansion and remodeling leads to crowding in the fixed bony orbit and this may have long term sequelae potentially irreversible damage can include propped Asus strabismus corneal ulceration optic nerve compression, vision impairment such as diplo pia optic neuropathy or even blindness. Cross talk between I. G. F. One R. And T. S. H. R. As well as I. G. F. one are mediated immune function may play a critical role in the pathogenesis of t e. D. Understanding the cross talk may be vital to addressing this debilitating disease.
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