by Lauren Taylor from In The Cloud Copy
Autoimmune uveitis is a condition in which abnormal activation of the immune cells takes place within the eye, ultimately leading to the destruction of the healthy cells of the eye. This inflammatory process can be due to an autoimmune reaction to the body’s own healthy cells, or could be caused by an external stimulus. Symptoms of this condition include eye redness, eye pain, light sensitivity, blurred vision, dark, floating spots in the field of vision, or decreased vision. Symptoms of the disease can come on very suddenly for the patient. Uveitis can often lead to blindness.
There are many other diseases and conditions that can be associated with uveitis, including other autoimmune conditions. Some that are associated include AIDS, Behcet’s syndrome, multiple sclerosis, psoriasis, rheumatoid arthritis, tuberculosis, and ulcerative colitis. Treatment of uveitis typically involves attempts to eliminate inflammation, prevent additional tissue damage from occurring, restoring lost vision, and eliminating pain to the affected individual. Steroid treatment is often prescribed, but this can lead to other conditions such as ulcers, osteoporosis, cardiovascular disease, diabetes, and more.
The Role of Th17 and IL-17A
Th17 lymphocyte appears to be the main immune cell that is involved in the uveitis process. This cell produces cytokines, which are pro-inflammatory molecules. Th17 also produces IL-17A, which attracts neutrophils (a type of immune cell) that can ultimately lead to tissue damage. Th17 cells are also present and involved in the process of neuroinflammation, and are often seen in patients with multiple sclerosis. Even with this information, multiple studies on medications that work to block IL-17A have not helped patients with autoimmune uveitis.
Studying IL-17 and Its Effects
A team of researchers at the National Eye Institute (NEI), which is a part of the National Institutes of Health, are diving deeper into the role of IL-17 and its role in these autoimmune conditions. Researchers found that even without the IL-17, the tissue damage remained constant and other inflammatory molecules were present. Researchers found that when the IL-17A was removed from the Th17 cells, other inflammatory molecules were produced, still resulting in inflammation.
What researchers found was that when the IL-17A locks up with the Th17 cell receptors, a cascade of signaling takes place, ultimately leading to the production of interleukin-24 or IL-24, which is an anti-inflammatory molecule. The IL-24 ultimately suppresses the Th17 inflammatory response, which decreases or halts the production of proteins such as IL-17F, GM-CSF and IL-22. Ultimately, this means that if IL-17A is not produced, this loop doesn’t occur and the Th17 cells are producing inflammatory cytokines in greater quantity than is needed, ultimately leading to increased inflammation.
The suppression of IL-17A as a treatment option in uveitis and others have never been successful, even though these treatments have been largely successful in treating other autoimmune conditions. Researchers are suggesting that treatment in combination, involving both IL-17A and IL-24, would likely yield better results.
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