Folic acid deficiency and vision: a review

Sijilmassi, Ouafa

doi:10.1007/s00417-019-04304-3

Cited by 49 publications

(34 citation statements)

References 76 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Several mechanisms have been studied and are likely to contribute to the damage. Reduction in folate concentration has been related to homocysteine accumulation, which would cause retinal neuron death and consequently an alteration of retinal layers, leading to maculopathy, but also an alteration of fiber layer, and therefore a damage to the optic nerve [21]. Furthermore, folate is an essential component of the enzyme tetrahydrofolate reductase (THFR) which is primarily involved in oligodendrocyte maturation.…”

Section: Folic Acid (Vitamin B9)mentioning

confidence: 99%

Nutritional Optic Neuropathies: State of the Art and Emerging Evidences

et al. 2020

View full text Add to dashboard Cite

Nutritional optic neuropathy is a cause of bilateral, symmetrical, and progressive visual impairment with loss of central visual acuity and contrast sensitivity, dyschromatopsia, and a central or centrocecal scotoma. The clinical features are not pathognomonic, since hereditary and toxic forms share similar signs and symptoms. It is becoming increasingly common due to the widespread of bariatric surgery and strict vegetarian or vegan diets, so even the scientific interest has recently increased. In particular, recent studies have focused on possible pathogenetic mechanisms, and on novel diagnostic and therapeutic strategies in order to prevent the onset, make a prompt diagnosis and an accurate nutritional supplementation, and to avoid irreversible optic nerve atrophy. Nowadays, there is clear evidence of the role of cobalamin, folic acid, thiamine, and copper, whereas further studies are needed to define the role of niacin, riboflavin, and pyridoxine. This review aims to summarize the etiology, diagnosis, and treatment of nutritional optic neuropathy, and it is addressed not only to ophthalmologists, but to all physicians who could come in contact with a patient with a possible nutritional optic neuropathy, being a fundamental multidisciplinary approach.

show abstract

Section: Folic Acid (Vitamin B9)mentioning

confidence: 99%

Nutritional Optic Neuropathies: State of the Art and Emerging Evidences

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Hyper-homocysteinemia is connected to specific polymorphisms in FA metabolism-associated genes ( 199 ) and has been reported to occur in autoinflammatory BD patients ( 200 ). A role for FA in autoimmune uveitis is therefore recognized [for review see ( 201 )].…”

Section: What Does the Gut–central Nervous System Axis Imply For Thermentioning

confidence: 99%

Immune Privilege: The Microbiome and Uveitis

et al. 2021

View full text Add to dashboard Cite

Immune privilege (IP), a term introduced to explain the unpredicted acceptance of allogeneic grafts by the eye and the brain, is considered a unique property of these tissues. However, immune responses are modified by the tissue in which they occur, most of which possess IP to some degree. The eye therefore displays a spectrum of IP because it comprises several tissues. IP as originally conceived can only apply to the retina as it contains few tissue-resident bone-marrow derived myeloid cells and is immunologically shielded by a sophisticated barrier – an inner vascular and an outer epithelial barrier at the retinal pigment epithelium. The vascular barrier comprises the vascular endothelium and the glia limitans. Immune cells do not cross the blood-retinal barrier (BRB) despite two-way transport of interstitial fluid, governed by tissue oncotic pressure. The BRB, and the blood-brain barrier (BBB) mature in the neonatal period under signals from the expanding microbiome and by 18 months are fully established. However, the adult eye is susceptible to intraocular inflammation (uveitis; frequency ~200/100,000 population). Uveitis involving the retinal parenchyma (posterior uveitis, PU) breaches IP, while IP is essentially irrelevant in inflammation involving the ocular chambers, uveal tract and ocular coats (anterior/intermediate uveitis/sclerouveitis, AU). Infections cause ~50% cases of AU and PU but infection may also underlie the pathogenesis of immune-mediated “non-infectious” uveitis. Dysbiosis accompanies the commonest form, HLA-B27–associated AU, while latent infections underlie BRB breakdown in PU. This review considers the pathogenesis of uveitis in the context of IP, infection, environment, and the microbiome.

show abstract

“…Until we know in detail how IL-17 family members, secreted from MAIT cells, act as factors to promote tumor cell growth or to enhance tumor cell killing and MAIT activation, we cannot propose a safe intervention to antagonize or stimulate IL-17 production, secretion, and functions for cancer therapies. Given the fact that vitamins B2 and B9 are important for all mammalian cell metabolic functions, targeting the inhibition or activation of their receptors is unlikely to be beneficial for the inhibition or activation of MAIT cells [ 53 , 54 ].…”

Section: Mait Cells and Il-17 Family Membersmentioning

confidence: 99%

MR1-Restricted T Cells in Cancer Immunotherapy

Flores-Villanueva

Sobhani

Wang

et al. 2020

Cancers

View full text Add to dashboard Cite

Major histocompatibility complex class I-related (MR1) was first identified as a cell membrane protein involved in the development and expansion of a unique set of T cells expressing an invariant T-cell receptor (TCR) α-chain. These cells were initially discovered in mucosal tissues, such as the intestinal mucosa, so they are called mucosal-associated invariant T (MAIT) cells. MR1 senses the presence of intermediate metabolites of riboflavin and folic acid synthesis that have been chemically modified by the side-products of glycolysis, glyoxal or methylglyoxal. These modified metabolites form complexes with MR1 and translocate from the endoplasmic reticulum to the plasma membrane where MAIT cells’ TCRs recognize them. Recent publications report that atypical MR1-restricted cytotoxic T cells, differing from MAIT cells in TCR usage, antigen, and transcription factor profile, recognize an as yet unknown cancer-specific metabolite presented by MR1 in cancer cells. This metabolite may represent another class of neoantigens, beyond the neo-peptides arising from altered tumor proteins. In an MR1-dependent manner, these MR1-restricted T cells, while sparing noncancerous cells, kill many cancer cell lines and attenuate cell-line-derived and patient-derived xenograft tumors. As MR1 is monomorphic and expressed in a wide range of cancer tissues, these findings raise the possibility of universal pan-cancer immunotherapies that are dependent on cancer metabolites.

show abstract

Folic acid deficiency and vision: a review

Cited by 49 publications

References 76 publications

Nutritional Optic Neuropathies: State of the Art and Emerging Evidences

Nutritional Optic Neuropathies: State of the Art and Emerging Evidences

Immune Privilege: The Microbiome and Uveitis

MR1-Restricted T Cells in Cancer Immunotherapy

Contact Info

Product

Resources

About