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. Author manuscript; available in PMC: 2014 Nov 14.
Published in final edited form as: Eye Contact Lens. 2014 Jul;40(4):248–256. doi: 10.1097/ICL.0000000000000042

Figure 4.

Figure 4

The current hypothesis of relationship between DED and inflammation. DED inflammation comprises both innate and adaptive immunity. It starts with an acute innate immune in response to environmental and/or microbial stresses, leading to activation and maturation of antigen-presenting cells (APCs). The matured APCs migrate into regional lymph nodes to generate and maintain dry eye- and ocular-specific autoreactive CD4+-T cells, autoantibody secreting B cells, leading to the adaptive immunity. Th17 cells back to the ocular surface through efferent blood vessels to promote production of inflammatory mediators, lymphangiogenesis and pathogenic immunocytic infiltration, leading to further damage of the ocular surface and progression of a chronic cycle of inflammation. Thus, the key mechanism in DED-related inflammation is not innate or adaptive immunity per se, but a abnormal inflammatory cycle sustained by dysregulation of immune response.