ACAID as a potential therapeutic approach to modulate inflammation in neurodegenerative diseases

Toscano-Tejeida, Diana; Ibarra, Antonio; Phillips-Farfán, Bryan V.; Fuentes-Farías, A.L.; Meléndez‐Herrera, Esperanza

doi:10.1016/j.mehy.2016.01.006

Cited by 9 publications

(5 citation statements)

References 104 publications

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“…These results support the idea that the eyes may indeed prime systemic immune tolerance across the body. In agreement with this conclusion, the sensitization of the eye’s anterior chamber with a variety of antigens offers immunological protection against autoimmune diseases or reduces tissue damage after physical or vascular injury [ 104 , 105 , 106 , 107 , 108 , 109 , 110 , 111 , 112 , 113 , 114 ].…”

Section: Discussionmentioning

confidence: 63%

Looking beyond Self-Protection: The Eyes Instruct Systemic Immune Tolerance Early in Life

Villafán,

Gutiérrez-Ospina

2023

Brain Sciences

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The eyes provide themselves with immune tolerance. Frequent skin inflammatory diseases in young blind people suggest, nonetheless, that the eyes instruct a systemic immune tolerance that benefits the whole body. We tested this premise by using delayed skin contact hypersensitivity (DSCH) as a tool to compare the inflammatory response developed by sighted (S) and birth-enucleated (BE) mice against oxazolone or dinitrofluorobenzene at the ages of 10, 30 and 60 days of life. Adult mice enucleated (AE) at 60 days of age were also assessed when they reached 120 days of life. BE mice displayed exacerbated DSCH at 60 but not at 10 or 30 days of age. AE mice, in contrast, show no exacerbated DSCH. Skin inflammation in 60-day-old BE mice was hapten exclusive and supported by distinct CD8+ lymphocytes. The number of intraepidermal T lymphocytes and migrating Langerhans cells was, however, similar between S and BE mice by the age of 60 days. Our observations support the idea that the eyes instruct systemic immune tolerance that benefits organs outside the eyes from an early age. The higher prevalence of inflammatory skin disorders reported in young people might then reflect reduced immune tolerance associated with the impaired functional morphology of the eyes.

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Section: Discussionmentioning

confidence: 63%

Looking beyond Self-Protection: The Eyes Instruct Systemic Immune Tolerance Early in Life

Villafán,

Gutiérrez-Ospina

2023

Brain Sciences

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“…A further example is that the retinal exposure of welding flash is associated with increased incidence of PD (Willis, 2005). Conversely, an immune tolerance induced by eyes via administration of antigens into the anterior chamber could be used as a therapeutic approach to promote neuroprotection for neurodegenerative diseases (Farooq and Ashour, 2013;Toscano-Tejeida et al, 2016;Pineda-Rodriguez et al, 2017). Thus, it is reasonable to conclude that the retina may be intimately involved with the onset and progression of PD as a potential precipitating factor outside of the CNS.…”

Section: Introductionmentioning

confidence: 99%

Retinal Degeneration: A Window to Understand the Origin and Progression of Parkinson’s Disease?

Zhang

Yue

et al. 2022

Front. Neurosci.

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Parkinson’s disease (PD), the second most prevalent neurodegenerative disorder, manifests with motor and non-motor symptoms associated with two main pathological hallmarks, including the deterioration of dopaminergic cells and aggregation of alpha-synuclein. Yet, PD is a neurodegenerative process whose origin is uncertain and progression difficult to monitor and predict. Currently, a possibility is that PD may be secondary to long lasting peripheral affectations. In this regard, it has been shown that retinal degeneration is present in PD patients. Although it is unknown if retinal degeneration precedes PD motor symptoms, the possibility exists since degeneration of peripheral organs (e.g., olfaction, gut) have already been proven to antedate PD motor symptoms. In this paper, we explore this possibility by introducing the anatomical and functional relationship of retina and brain and providing an overview of the physiopathological changes of retinal structure and visual function in PD. On the basis of the current status of visual deficits in individuals with PD, we discuss the modalities and pathological mechanism of visual function or morphological changes in the retina and focus on the correlation between visual impairment and some representative structural features with clinical significance. To consider retinal degeneration as a contributor to PD origin and progress is important because PD evolution may be monitored and predicted by retinal studies through state-of-the-art techniques of the retina. It is significant to integrally understand the role of retinal morphological and functional changes in the neurodegenerative process for the diagnosis and therapeutic strategies of PD.

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“…In any case, these F4/80 + CD11b + ocular APCs migrate to the thymus and induce the generation of NKT cells (NK1.1 + CD4 − CD8 − ), which, in turn, play a role in producing splenic suppressor cells. In the marginal zone (MZ) of the spleen, F4/80 + CD11b + APCs emigrating from the eye also interact with various types of cells and molecules, helping to generate immunomodulatory cells, such as CD8 + or CD4 + regulatory T cells (Tregs), MZ regulatory B cells, γδ Tregs, iNKT, and NKT regulatory cells, which spread throughout the body and induce antigen-specific immune deviation ( 4 ). Among the immunologic hallmarks of ACAID are its inhibition, first, of the initial activation and differentiation of T cells into Th1 effector cells (mainly characterized by secretion of IFNγ, TNFα, and IL-2), and second, of the expression of Th1-mediated immunity, such as delayed-type hypersensitivity (DTH) and skin allograft rejection ( 5 ).…”

Section: Introductionmentioning

confidence: 99%

Cellular and Molecular Mechanisms of Anterior Chamber-Associated Immune Deviation (ACAID): What We Have Learned from Knockout Mice

2017

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Anterior chamber-associated immune deviation (ACAID) is a well-known phenomenon that can occur after an antigen is introduced without any danger signal into the anterior chamber of a murine eye. It is reported to lead to an antigen-specific immune deviation throughout the body. Despite the relatively little evidence of this phenomenon in humans, it has been suggested as a potential prophylactic strategy in allograft rejections and in several autoimmune diseases. Cellular and molecular mechanisms of ACAID have been explored in different murine models mainly as proofs of concept, first by direct analyses of immune components in normal immunocompetent settings and by cell transfer experiments. Later, use of knockout (KO) mice has helped considerably to decipher ACAID mechanisms. However, several factors raise questions about the reliability and validity of studies using KO murine models. This mini-review summarizes results obtained with KO mice and discusses their advantages, their potential weaknesses, and their potential methods for further progress.

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ACAID as a potential therapeutic approach to modulate inflammation in neurodegenerative diseases

Cited by 9 publications

References 104 publications

Looking beyond Self-Protection: The Eyes Instruct Systemic Immune Tolerance Early in Life

Looking beyond Self-Protection: The Eyes Instruct Systemic Immune Tolerance Early in Life

Retinal Degeneration: A Window to Understand the Origin and Progression of Parkinson’s Disease?

Cellular and Molecular Mechanisms of Anterior Chamber-Associated Immune Deviation (ACAID): What We Have Learned from Knockout Mice

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