Pigment Epithelium–Derived Factor Enhances the Suppressive Phenotype of Regulatory T Cells in a Murine Model of Dry Eye Disease

Singh, Rohan Bir; Blanco, Tomás; Mittal, Sanjay; Alemi, Hamid; Chauhan, Sunil; Chen, Yihe; Dana, Reza

doi:10.1016/j.ajpath.2021.01.003

Cited by 14 publications

(3 citation statements)

References 51 publications

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“…Their subsequent experiments showed that in vitro culture in the presence of PEDF prevented the reduction in frequency and phenotypic inhibition of regulatory T cells induced by proinflammatory cytokines (associated with helper T cells type 17) in normal mice. Their results revealed that PEDF can promote the inhibitory ability of regulatory T cells and reduce its type 17 helper T cellmediated dysfunction, thus playing a role in DED inhibition (Singh et al, 2021). Recently, Ma et al found that PEDF could inhibit the expression of inflammatory cytokines IL-1β, IL-6, TNF-α, and IL-17A in DED and the percentage of Th17 cells in vivo and in vitro experiments.…”

Section: Immunoregulatory Molecules and Inflammationmentioning

confidence: 98%

Recent Developments About the Pathogenesis of Dry Eye Disease: Based on Immune Inflammatory Mechanisms

Dong

et al. 2021

Front. Pharmacol.

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Dry eye disease is a common and frequently occurring ophthalmology with complex and diverse causes, and its incidence is on the upward trend. The pathogenesis of DED is still completely clear. However, the immune response based on inflammation has been recognized as the core basis of this disease. In this review, we will systematically review the previous research on the treatment of DED in immune inflammation, analyze the latest views and research hotspots, and provide reference for the prevention and treatment of DED.

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Section: Immunoregulatory Molecules and Inflammationmentioning

confidence: 98%

Recent Developments About the Pathogenesis of Dry Eye Disease: Based on Immune Inflammatory Mechanisms

Dong

et al. 2021

Front. Pharmacol.

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“…[ 85 ] This could possibly due to the immune cell assessment was done using the whole eye tissue rather than ocular surface tissue in the animal study. [ 85 ] In addition to immune cell alterations on the ocular surface, higher proportions of CD4 + T cells,[ 86 , 93 , 94 ] Th1 cells,[ 89 ] Th17 cells,[ 67 , 92 , 95 , 96 ] activated T cells,[ 89 , 97 ] and autoreactive T cells[ 63 ] and lower number of Tregs[ 86 , 98 ] have also been seen in the draining lymph nodes of animal with DED. Most of the human and animal studies have demonstrated strong association or direct mechanism that underpins T cells in mediating ocular surface inflammation in DED.…”

Section: Ocular Surface Immune Cell Profile In Dedmentioning

confidence: 99%

“…[ 37 , 38 ] PPAR-alpha agonist, fenofibrate, resulted in alleviation of DED severity in animal models by reducing Th17 and enhancing Treg cells. [ 95 ] Treg-recruiting microspheres[ 86 ] and PEDF[ 98 ] were shown to recruit and enhance immunosuppressive ability of Treg cells leading to amelioration of DED like features in animal models. Combined light therapy (intense pulsed light – IPL and low-level light therapy – LLLT) reduced the proportion of B cells on the ocular surface of DED patients with meibomian gland dysfunction.…”

Section: Ocular Surface Immune Cell Profile In Dedmentioning

confidence: 99%

Ocular surface immune cell diversity in dry eye disease

Nair

D’Souza²,

Khamar³

et al. 2023

Indian Journal of Ophthalmology

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Dry eye disease (DED) is a multifactorial chronic ocular surface inflammatory condition. Disease severity has been directly related to the immuno-inflammatory status of the ocular surface. Any perturbation in the orchestrated functional harmony between the ocular surface structural cells and immune cells, both resident and trafficking ones, can adversely affect ocular surface health. The diversity and contribution of ocular surface immune cells in DED have been of interest for over a couple of decades. As is true with any mucosal tissue, the ocular surface harbors a variety of immune cells of the innate-adaptive continuum and some of which are altered in DED. The current review curates and organizes the knowledge related to the ocular surface immune cell diversity in DED. Ten different major immune cell types and 21 immune cell subsets have been studied in the context of DED in human subjects and in animal models. The most pertinent observations are increased ocular surface proportions of neutrophils, dendritic cells, macrophages, and T cell subsets (CD4+; CD8+; Th17) along with a decrease in T regulatory cells. Some of these cells have demonstrated disease-causal association with ocular surface health parameters such as OSDI score, Schirmer’s test-1, tear break-up time, and corneal staining. The review also summarizes various interventional strategies studied to modulate specific immune cell subsets and reduce DED severity. Further advancements would enable the use of ocular surface immune cell diversity, in patient stratification, i.e. DED-immunotypes, disease monitoring, and selective targeting to resolve the morbidity related to DED.

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