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. Author manuscript; available in PMC: 2021 Oct 28.
Published in final edited form as: Ocul Surf. 2020 May 26;19:157–168. doi: 10.1016/j.jtos.2020.05.009

Figure 1: In the afferent arm of the Th17 response, activated APCs are poised to migrate from the ocular surface to the draining lymphoid tissue.

Figure 1:

In homeostatic conditions, the cornea contains a heterogenous population of immature antigen presenting cells (iAPCs) with limited capacity to stimulate T cells. However, these cells acquire MHC class II, CD80 and CD86 expression on exposure to inflammatory stress to generate mature APCs (mAPCs). The upregulated expression of MHC class-II and costimulatory molecules has been attributed to IL-1, IL-6, and TNF-α from corneal epithelial cells, Substance P (SP) from the corneal nerves, and granulocyte-macrophage colony-stimulating factor (GM-CSF) from Th17 cells (not shown in the figure). Regarding immunoregulatory factors, various molecules including PD-L1, LXA4, PEDF, and TSP-1 derived from corneal epithelium, VIP and PACAP expressed by corneal nerves, and αMSH from the aqueous humor play an immunosuppressive role by limiting inflammatory cytokine-induced APC maturation. The chemokine receptor CCR7 expressed by mature APCs directs their trafficking to the lymph nodes via newly formed corneal lymphatic vessels.