The Role of Th17 Cells and IL-17 in Th2 Immune Responses of Allergic Conjunctivitis

Abstract

Allergic conjunctivitis (AC) is a common allergic disease that is often associated with the onset of rhinitis or asthma. The incidence of AC has increased significantly in recent years possibly due to air pollution and climate warming. AC seriously affects patients' quality of life and work efficiency. Th (T-helper) 2 immune responses and type I hypersensitivity reactions are generally considered the basis of occurrence of AC. It has been found that new subpopulations of T-helper cells, Th17 cells that produce interleukin-17 (IL-17), play an important role in the Th2-mediated pathogenesis of conjunctivitis. Studies have shown that Th17 cells are involved in a variety of immune inflammation, including psoriasis, rheumatoid arthritis, inflammatory bowel disease, systemic lupus erythematosus, and asthma. However, the role of Th17 and IL-17 in AC is unclear. This paper will focus on how T-helper 17 cells and interleukin-17 are activated in the Th2 immune response of allergic conjunctivitis and how they promote the Th2 immune response of AC.

Figure 1

In classical type I hypersensitivity reactions, activation of individual cells and immune molecules finally results in mast cell degranulation and eosinophil infiltration. Factors such as IL-3, IL-4, IL-5, and IL-13 produced by Th2 cells promote this process.

Figure 2

1. CD40 and CD86 signaling on DC appears to be critical in the induction of Th17 cells. 2. IL-23 supports the maintenance of Th17 cell function. 3. IL-6 and TGF-β produced by eosinophil and DC expression promote Th17 cell differentiation. 4. Activated Th2 cells can be directly transformed into Th17 cells.

Figure 3

1. The immune response is maintained by the IL-23-GM-CSF axis. 2. IL-17A and IL-17F can promote the production of eosinophils CXCL1, IL-8, and CCL4, as well as IL-1β and IL-6. 3. IL-17A is involved in the pathophysiology of allergies by increasing the ability of IL-13 to activate signaling pathways such as intracellular STAT-6. IL-17A protein expression synergizes with IL-13. 4. Th17 cells have been shown to help B cell differentiation and to play a key role in the formation of ectopic lymphoid follicles in the target organ.