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The roles of macrophage migration inhibitory factor in retinal diseases
Hongbing Zhang1, Xianjiao Zhang2, Hongsong Li3
1Shaanxi Institute of Ophthalmology, Xi'an; Department of Ophthalmology, First Affiliated Hospital of Northwest University, Xi'an, Shaanxi Province, China.
Abstract:
Macrophage migration inhibitory factor (MIF), a multifunctional cytokine, is secreted by various cells and participates in inflammatory reactions, including innate and adaptive immunity. There are some evidences that MIF is involved in many vitreoretinal diseases. For example, MIF can exacerbate many types of uveitis; measurements of MIF levels can be used to monitor the effectiveness of uveitis treatment. MIF also alleviates trauma-induced and glaucoma-induced optic nerve damage. Furthermore, MIF is critical for retinal/choroidal neovascularization, especially complex neovascularization. MIF exacerbates retinal degeneration; thus, anti-MIF therapy may help to mitigate retinal degeneration. MIF protects uveal melanoma from attacks by natural killer cells. The mechanism underlying the effects of MIF in these diseases has been demonstrated: it binds to cluster of differentiation 74, inhibits the c-Jun N-terminal kinase pathway, and triggers mitogen-activated protein kinases, extracellular signal-regulated kinase-1/2, and the phosphoinositide-3-kinase/Akt pathway. MIF also upregulates Toll-like receptor 4 and activates the nuclear factor kappa-B signaling pathway. This review focuses on the structure and function of MIF and its receptors, including the effects of MIF on uveal inflammation, retinal degeneration, optic neuropathy, retinal/choroidal neovascularization, and uveal melanoma.
Insights
Macrophage migration inhibitory factor (MIF) plays a key role in various eye diseases, influencing inflammation, neovascularization, and degeneration. Understanding MIF
Area of Science:
- Ophthalmology
- Immunology
- Molecular Biology
Background:
- Macrophage migration inhibitory factor (MIF) is a crucial cytokine involved in immune responses and inflammation.
- Evidence suggests MIF's involvement in several vitreoretinal diseases, impacting their pathogenesis and progression.
Purpose of the Study:
- To review the structure and function of MIF and its receptors.
- To elucidate the role of MIF in various ocular conditions, including uveitis, optic neuropathy, neovascularization, and uveal melanoma.
Main Methods:
- Literature review focusing on studies investigating MIF's role in ocular diseases.
- Analysis of molecular mechanisms, including receptor binding and signaling pathways activated by MIF.
Main Results:
- MIF exacerbates uveitis and retinal degeneration but alleviates optic nerve damage.
- MIF is critical for retinal/choroidal neovascularization and protects uveal melanoma from immune attack.
- MIF exerts its effects by binding to CD74 and modulating pathways like JNK, MAPK, PI3K/Akt, TLR4, and NF-κB.
Conclusions:
- MIF is a significant factor in the pathophysiology of diverse vitreoretinal diseases.
- Targeting MIF presents a potential therapeutic strategy for managing inflammatory and degenerative ocular conditions.
