The dysregulation of immune response in uveitis. (IMAGE)
Caption
Uveitis results from imbalance between inflammatory mechanisms and regulatory mechanisms. Several immune cells are involved in this process. The balance between T helper 17 (Th17) cells and regulatory T cells (Tregs) is crucial for maintaining immune homeostasis and preventing the development of autoimmune disorders in uveitis. Effector B cells can produce pro-inflammatory cytokines, such as interleukin-6 (IL-6), interferon-γ (IFN-γ), and granulocyte-macrophage colony-stimulating factor (GM-CSF), which play a role in promotion of inflammation, and activation of other immune cells. M1 macrophages are typically associated with pro-inflammatory responses and is crucial for the pathological of uveitis. The over activation of Th1/Th17, B cells and M1 macrophages results in the breaking down of the blood‒retinal barrier and, consequently, different inflammatory cells such as monocytes, granulocytes, and non-specific lymphocytes from the circulation are recruited. These infiltrating inflammatory cells develop inflammation and further destroy the ocular tissue.
Credit
Shengping Hou
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