This article [Streilein et al., 2000: (http://www.ncbi.nlm.nih.gov/pubmed/11268357)] is fantastic, and the authors discuss anterior chamber-associated immune deviation (ACAID) ("ocular immune privilege") in relation to neuropeptide (CGRP, VIP, alpha-MSH, etc.) release by nerve fibers innervating the iris and ciliary body. I'm not entirely clear on the mechanisms, but I think ACAID is essentially similar, in some ways, to the systemic immunosuppression induced by UVB. The neuropeptides reduce the costimulatory capacities of antigen-presenting cells migrating from the eyes and thereby cause antigen-specific tolerance that's mediated by regulatory T-cells, I think. CGRP also can directly inhibit some functions of resident (?) macrophages or of monocytes infiltrating the eyes, etc. There's the "lymphatic" drainage of aqueous humor into the circumferential veins (meaning there's the absence of lymphatic drainage and of the potentially-pro-inflammatory APC maturation-inducing signals and mechanisms, taking place in lymph nodes, for some of these antigen-presenting cells migrating from the eyes) and into the spleen that's a key factor in ACAID (animals have to have an intact spleen to develop ACAID in some of these experiments). Some interesting classes of regulatory T-cells, such as natural-killer T-cells (in this case, they're like "immunosuppressive loose cannons" or something, because I think the functions of natural killer T-cells are only very loosely regulated), appear in the spleen following UVB, but I don't think (as far as I know, it's not) that the spleen is required for UVB-induced systemic immunosuppression. In any case, on pages 302-303, Streilein et al. (2000) suggest that long periods of darkness (of 48 hours or longer) cause the effects of melatonin on antigen-presenting cells at different points in the eye to become dominant over the effects of transforming growth factor-beta2 (TGFb2) and decrease or interfere with the maintenance of ACAID. It's interesting that there's thought to be a vitamin D response element (VDRE) in the TGFb2 promoter [as discussed in Lamprecht et al., 2003: (http://www.ncbi.nlm.nih.gov/pubmed/12894248); (http://scholar.google.com/scholar?hl=en&q=%22vitamin+D%22+VDRE+TGF+beta2+promoter)], and TGFb2 and many other aspects of TGFb2 signalling are, in my view, strongly interconnected with vitamin D receptor (VDR) signalling. (It's difficult to search on Greek letters in that search engine, and there's probably some trick, to doing it, that I'm not aware of.) Streilein et al. (2000) also discuss the fact that visible light in the green wavelengths (500-510) is thought to contribute to the maintenance of ACAID. Here's a section in which Streilein et al. (2000) discuss their thoughts on ACAID in relation to primary afferent neurons (the reason I couldn't include this in the paper, for example, despite its similarity to the research on the CGRP-dependence of UVB-induced systemic immunosuppression, is that explaining these researchers' thoughts on the role of trigeminal fibers, innervating the cornea, in the visible-light-mediated maintenance of ACAID would have required another two pages to even convey what mechanisms could account for this type of effect--and I'm still not sure what the mechanism would be, though I think the UVB-mediated mechanisms seem more clear than those that would explain the actions of visible light):
"The capacity of the normal eye to support ACAID induction is dependent upon integrity of afferent nerves from the cornea, as is the ability of iris and ciliary body to secrete an immunosuppressive ocular microenvironment. We suspect that tonic signals arise from the corneal surface. These signals are propagated through the trigeminal ganglion to the central nervous system, where they promote, via connections to the nervous supply of the iris and ciliary body, the intraocular secretion of immunomodulatory neuropeptides" (Streilein et al., 2000, p. 302).
The pathways are not clearly defined at all, though. I don't see how visible light could induce action potentials in trigeminal ganglion neurons innervating the corneal surfaces, as UVB does. Streilein et al. (2000) noted that researchers had found that transection of the optic nerve hadn't abolished the visible light-mediated maintenance of ACAID. I have little doubt that visible light does contribute to ACAID, and it may be that the pathway involves some circuitous pathway involving the preganglionic cholinergic neurons in the Edinger-Westphal nucleus. I don't know very much about the anatomy. Here's a search on visible light and ACAID (http://scholar.google.com/scholar?q=visible+light+%22immune+deviation%22+OR+%22immune+privilege%22&hl=en)]. That's not a very revealing search, and maybe some researchers have researched mechanisms, without explicit discussions of the immunological implications, by which visible light can influence VIP and CGRP release. I don't know if there are anatomical pathways by which retinal ganglion cells, activated in response to visible wavelengths, can influence, independently of the optic nerve, different classes of neurons in the suprachiasmatic nucleus or other parts of the brain. These authors don't discuss the possible anatomical pathways very much [Warren et al., 2003: (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2435209)(http://www.ncbi.nlm.nih.gov/pubmed/12752771)], but maybe visible light can induce neuropeptide release from the peripheral terminals of trigeminal ganglion neurons by some polysynaptic pathway(s) that do not require transmission along optic nerve fibers. Or maybe the "efferent" arm of the visible-light-induced release of VIP and CGRP into the iris and ciliary body requires the indirect actions of ciliary ganglion neurons on trigeminal ganglion neurons innervating those parts of the eye (I mean that a ciliary ganglion neuron innervating the iris and ciliary body might depolarize and induce afferent action potentials in "one" trigeminal ganglion neuron and thereby induce a dorsal root reflex that would induce an efferent action potential in a second TG neuron and thereby release CGRP into the iris, etc.). Maybe that's not possible, but I'm just suggesting that it might not be necessary for the polysynaptic pathway, induced by the supposed optic-nerve-independent actions of visible light, to influence TG neurons by actions on the central terminals of TG neurons in the caudal trigeminal nucleus. I don't know, and the anatomy is really complex and not all that well-understood, it seems. I'm not trying to say that "anything goes" as far as the anatomical pathways are concerned. I'm just discussing the topic openly. Berson et al. (2003) (http://scholar.google.com/scholar?hl=en&q=%22Strange+vision%3A+ganglion+cells+as%22+Berson) discussed the fact that some intrinsically-photosensitive retinal ganglion cells project to and form direct synaptic connections with neurons in the olivary pretectal nucleus and thereby influence the firing rates of preganglionic neurons in the Edinger-Westphal nucleus and, as a result, also the firing rates of ciliary ganglion neurons. Vakapoulos (2005) [Vakalopoulos, 2005: (http://scholar.google.com/scholar?hl=en&q=Vakalopoulos+%22the+unconscious%3A+A+proposal+for+the%22)] discussed some of the ways in which retinal ganglion cells could influence visual "perceptions," of one kind or another, in blind people. Even though the effects of visible light on ACAID can, apparently, occur independently of transmission by optic nerve fibers, it seems that there could be both optic-nerve-dependent and independent pathways by which neurons in the ciliary ganglia could, via synaptic inputs to neurons in the Edinger-Westphal from neurons in the suprachiasmatic nucleus, participate in ACAID [(http://scholar.google.com/scholar?hl=en&q=%22edinger+westphal%22+preganglionic+suprachiasmatic); (http://scholar.google.com/scholar?hl=en&q=%22ciliary+ganglion%22+%22anterior+chamber%22+iris+%22ciliary+body%22)].
I think I remember seeing someone discussing something about the capacity of retinal ganglion cell activation to mediate circadian effects independently of transmission by optic nerve fibers, but I might well be wrong about that. Warren et al. (2003) discuss the fact that the action potentials induced in retinal ganglion cells, in response to their depolarization by visible wavelengths, seem to suggest the involvement of a photoreceptive protein that's a member of the transient receptor potential family of ion channels that can serve as photoreceptors in invertebrates (http://scholar.google.com/scholar?hl=en&q=TRP+%22transient+receptor+potential%22+%22retinal+ganglion+cells%22). It's interesting that capsaicin induces action potentials in C-fibers by binding to the type 1 vanilloid receptor (VR1), which is a member of the family of TRP channels in humans and other mammals. That's not much of a statement and doesn't mean anything, by itself, but it seems as if there's some crude overlap between some of these primitive mechanisms and the mechanisms that operate in higher mammals.
I was initially going to mention, again, the possibility that small amounts of UVB or UVA had been in the light sources that researchers had used to evaluate visible-light-mediated ACAID maintenance, but it sounds like they used very specific wavelengths within the visible spectrum.
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