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. 2022 Jan 17;8:815075. doi: 10.3389/fmed.2021.815075

Figure 1.

Figure 1

The immunoinflammatory response of the ocular surface in dry eye disease. Desiccating, oxidative and hyperosmolarity stress activate cell signaling pathways at the ocular surface, which leads to the production of pro-inflammatory cytokines (TNF-α, IL-1β and IL-6) and matrix metalloproteinase (mainly MMP9). These factors promote the maturation of antigen-presenting cells and allow mature antigen-presenting cells to migrate to the lymph nodes through the afferent lymphatic vessels. In the lymph nodes, mAPCs induce effector T cells (Th 1 and Th17) and recruit them to migrate to the ocular surface. Meanwhile, mAPCs activate the NLRP3 inflammasome, promotes the secretion of IL-1β and IL-18, and further aggravates the ocular surface inflammation. MAPK, mitogen-activated protein kinase; JNK, Jun N-terminal kinase; ERK, extracellular regulated protein kinase; NF-κB, nuclear transcription factor-κB; MMPs, matrix metalloproteinases; TNF-α, tumor necrosis factor-α; IL, interleukin; IFN-γ, interferon-γ; NLRP3, NLR family pyrin domain containing 3; TGF-β, transforming growth factor β; Th, T helper; Treg, regulatory T cell; LFA-1, lymphocyte function associated antigen 1; ICAM-1, intercellular adhesion molecule 1; APC, antigen presenting cell; mAPC, mature antigen presenting cell; ASC, apoptosis speck-like protein.