daisybell
Senior Member
- Messages
- 1,613
- Location
- New Zealand
Has anyone else had problems with floaters and/or uveitis associated with their ME?
I have just been diagnosed with multiple floaters in one of my eyes - apparently far exceeding what is normal for my age. I am very short-sighted but am wondering if this could be an auto-immune issue and if so, is the ME the culprit?
I found the following info (on Wikipedia):
Onset of Uveitis can broadly be described as a failure of the Ocular immune system and the disease results from inflammation and tissue destruction. Uveitis is driven by the Th17 T cell sub-population that bear T-cell receptors specific for proteins found in the eye.[9]These are often not deleted centrally whether due to ocular antigen not being presented in the thymus (therefore not negatively selected) or a state of anergy is induced to prevent self targeting.[10][11]
Autoreactive T cells must normally be held in check by the suppressive environment produced by Microglia and dendritic cells in the eye.[12] These cells produce large amounts of TGF beta and other suppressive cytokines, including IL-10, to prevent damage to the eye by reducing inflammation and causing T cells to differentiate to inducible T reg cells. Innate immune stimulation by bacteria and cellular stress is normally suppressed by myeloid suppression while inducible Treg cells prevent activation and clonal expansion of the autoreactive Th1 and Th17 cells that possess potential to cause damage to the eye.
Whether through infection or other causes, this balance can be upset and autoreactive T cells allowed to proliferate and migrate to the eye. Upon entry to the eye, these cells may be returned to an inducible Treg state by the presence of IL-10 and TGF-beta from microglia. Failure of this mechanism leads to neutrophil and other leukocyte recruitment from the peripheral blood through IL-17secretion. Tissue destruction is mediated by non-specific macrophage activation and the resulting cytokine cascades.[13] Serum TNF-α is significantly elevated in cases while IL-6 and IL-8 are present in significantly higher quantities in the Aqueous humour in patients with both quiescent and active uveitis.[14] These are inflammatory markers that non-specifically activate local macrophages causing tissue damage.
Any thoughts appreciated!
I have just been diagnosed with multiple floaters in one of my eyes - apparently far exceeding what is normal for my age. I am very short-sighted but am wondering if this could be an auto-immune issue and if so, is the ME the culprit?
I found the following info (on Wikipedia):
Onset of Uveitis can broadly be described as a failure of the Ocular immune system and the disease results from inflammation and tissue destruction. Uveitis is driven by the Th17 T cell sub-population that bear T-cell receptors specific for proteins found in the eye.[9]These are often not deleted centrally whether due to ocular antigen not being presented in the thymus (therefore not negatively selected) or a state of anergy is induced to prevent self targeting.[10][11]
Autoreactive T cells must normally be held in check by the suppressive environment produced by Microglia and dendritic cells in the eye.[12] These cells produce large amounts of TGF beta and other suppressive cytokines, including IL-10, to prevent damage to the eye by reducing inflammation and causing T cells to differentiate to inducible T reg cells. Innate immune stimulation by bacteria and cellular stress is normally suppressed by myeloid suppression while inducible Treg cells prevent activation and clonal expansion of the autoreactive Th1 and Th17 cells that possess potential to cause damage to the eye.
Whether through infection or other causes, this balance can be upset and autoreactive T cells allowed to proliferate and migrate to the eye. Upon entry to the eye, these cells may be returned to an inducible Treg state by the presence of IL-10 and TGF-beta from microglia. Failure of this mechanism leads to neutrophil and other leukocyte recruitment from the peripheral blood through IL-17secretion. Tissue destruction is mediated by non-specific macrophage activation and the resulting cytokine cascades.[13] Serum TNF-α is significantly elevated in cases while IL-6 and IL-8 are present in significantly higher quantities in the Aqueous humour in patients with both quiescent and active uveitis.[14] These are inflammatory markers that non-specifically activate local macrophages causing tissue damage.
Any thoughts appreciated!