The complement system is an important defense mechanism in both innate and adaptive immunity, whose activation leads to cleavage of components and fixation and attachment to pathogens. Complement system activation has been established to be associated with ocular diseases (Clark and Bishop, 2018, Ma et al., 2022, Sohn et al., 2007), and is considered to be involved in myopia progression in recent years (Gao et al., 2015, Garcia-Gen et al., 2021, Riddell and Crewther, 2017).

Complement decay accelerating factor (CD55), also known as the decay-accelerating factor (DAF), is a surface-intrinsic regulatory protein expressed in the complementary system and acts as complement inhibitor to modulates of complement 3 (C3) and complement 5 (C5) convertases, further suppress the complement activation, and has also been found to be associated with T cell activation (Heeger et al., 2005, Esposito et al., 2010, Cocuzzi et al., 2001). CD55 was found as a myopia-related gene in 3712 healthy Japanese volunteers in a previous study using per-single-nucleotide polymorphism analysis (Yoshikawa et al., 2014). Although the association between the complement pathway and myopia has been discussed in different animal and human myopic models (Gao et al., 2015, Long et al., 2013, Giummarra et al., 2018), concrete research on their relationship is still sparse. In this study, we evaluated changes in CD55 levels in different myopia models and demonstrated the correlation between inflammatory cytokines, the complementary system, and CD55. We further hypothesized that CD55 plays a significant role in myopia progression and may suppress eye inflammatory responses and inhibit myopia progression.