Investigative Ophthalmology & Visual Science, Vol. 33, No. 5, April 1992
Copyright © Association for Research in Vision and Ophthalmology
The Wavelength of Light Governing
Intraocular Immune Reactions
Thomas A. Ferguson,*f Sheela L. Mahendra,* Philip Hooper,* and Henry J. Kaplan*
Injection of antigen into the anterior chamber of the eye results in the induction of suppressed systemic
cell-mediated responses as measured by delayed-type hypersensitivity or contact hypersensitivity
(CHS). Previous studies from the authors' laboratories have determined that this response is governed
by exposure of the eye to visible light during the initial intraocular encounter between T cells and
antigen. To more fully understand the role of light, as well as to begin to understand the molecular
mediators involved, the authors chose to explore the properties of light governing the effect. Neutral
density filter were used to demonstrate that the minimum amount of light required to induce suppression of CHS following anterior chamber injection of antigen is 1-2 lux (lumens/meter2). With narrow
band filters, the wavelengths responsible for suppression were shown to be 500-510 nm. The results
show that the effect of light extends beyond the hapten-derivatized spleen cell system to other antigens
placed in the anterior chamber of the eye. Studies also show that the retina and the pineal gland, two
light absorbing structures, may not be involved. The results in this report show that light of very
restricted wavelengths controls intraocular immune reactions. Invest Ophthalmol Vis Sci 33:
1788-1795,1992
We have been studying the consequences of presenting antigen to the immune system via the anterior
chamber of the eye. The results of our studies,1"5 with
those of other laboratories,6"9 suggest that a unique
environment exists in the eye that modulates the pattern of responses generally observed when antigen is
encountered subsequently at other sites. An important model for studying intraocular immune reactions is anterior chamber associated immune deviation (ACAID).4 In this system, the injection of antigens into the anterior chamber of the eye induces a
consistent pattern of systemic responses characterized
by the induction of antigen specific suppression for
delayed type hypersensitivity (DTH) or contact hypersensitivity (CHS).1"9 Simultaneously, antibody production is normal or elevated.6
We previously showed that down regulation of
CHS following anterior chamber injection of 2,4,6From the *Department of Ophthalmology and Visual Sciences
and the fDepartment of Pathology, Washington University School
of Medicine, St. Louis, Missouri.
This work was supported by NIH grants EY06765 and EY08972
as well as a Department of Ophthalmology and Visual Sciences
grant from Research to Prevent Blindness, Inc., New York, New
York.
Submitted for publication: July 19, 1991; accepted October 23,
1991.
Reprint requests: Dr. Thomas A. Ferguson, Department of Ophthalmology and Visual Sciences, Washington University School of
Medicine, St. Louis, MO 63110.
trinitrophenol-coupled spleen cells (TNP-Spl) is initiated by the activation of certain T cells within the
eye,2 leading to the elaboration of an inhibitory molecule from the eye that causes the activation of T cells
in the spleen. By using dark-reared and light-reared
mice (Balb/c), we established that visible light directly
affects this intraocular phenomenon.3 If light was prevented from reaching the eye by dark-rearing, by placing light-reared animals in the dark post anterior
chamber injection, or by closing the eyelid of lightreared animals post anterior chamber injection,
ACAID is not established. Furthermore, we demonstrated that visible light—not ultraviolet (UV) or infrared—was responsible for the observed effects and that
the effect of light on the eye was not developmentally
mandated (as is visual development), but was inducible in adult dark-reared animals. These results suggest that light entering the eye establishes the conditions necessary for the induction of suppressed CHS
by influencing the intraocular T cell reactions that
initiate suppression.
To further examine the effect of light on the eye, we
sought to determine the amount of light required, as
well as an action spectrum, for the observed effects.
Studies also were done to evaluate a role for the retina
and the pineal gland, as well as to extend the phenomenon to other antigens. These studies have important
implications for understanding intraocular immune
regulation and determining the molecular mediators
that regulate intraocular immune responses.
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No. 5
LIGHT REGULATION OF ACAID / Ferguson er ol
Materials and Methods
Mice
Balb/cByJ, C3H/HeJ (rd/rd; [rd for retinal degeneration]), and CBA/J mice were purchased from Jackson Labs, Bar Harbour, ME. In all in vivo experiments, groups consisted offiveor more animals. Animals were used when they were 6-10 wk old. Balb/c
mice that were neonatally pinealectomized and shamoperated mice were purchased from Taconic Farms
(Germantown, NY) when they were 4-6 wk old. Animal experiments were performed in compliance with
the ARVO Resolution on the Use of Animals in Research.
Construction of Boxes for Wavelength
Determinations
Boxes were constructed and fitted with special
filters to control the delivery of light to animals in our
experiments. Wratten photographic filters were purchased from Kodak Co., Rochester, NY. Two X two
inch filters that cover the visible spectrum from 400700 nm were purchased from Oriel Corp., Stratford,
CT. Each filter transmits 95% of its light within 5 nm
of the optimum wavelength. The light sources were
halogen beam automobile headlights (Western Auto,
Fenton, MO) powered by a standard 12 V power
source equipped with a rheostat. The power source
was connected to a timer switch so the appropriate
wavelength was delivered on a 12 hr light/12 hr dark
cycle. Light was focused through the 2 x 2 inch filters
fitted in the top of a box. Each light illuminated a cage
containing five mice. The amount of light was adjusted with the rheostat on the power source and was
standardized for each experiment with a photometer
so all mice received the same amount of light regardless of the filter used.
Photometric Measurements of Light
Because our phenomenon was governed by the response to light in the visible range, we chose to study
light using photometric measurements and to standardize our experiments using a photometer. Photometry measures the visible light as the eye can respond
to it. The measurement is expressed in lumens/meter2
or lux. Measurement in lux gives the amount of
power emitted from a source per unit of surface area.
Because different wavelengths have different energies,
we tried to standardize our light source and the number of lumens the eye received in the visible range. A
mouse cage was centered in the box 3-'/2 inches below
thefilter.The photometer then was placed on the bottom of the cage and zeroed. The amount of light was
adjusted with the rheostat on the power source. We do
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1789
not believe that the effect of light on ACAID was related solely to the amount of light energy. The reason
is that the action spectrum falls in the visible range,
with UV and blue (lower energy) and infrared and red
(higher energy) having no effect.3
Antigens
2,4,6 Trinitrobenzene sulfonic acid (TNBS), pigeon
cytochrome-C, and hen egg lysozyme (HEL) were obtained from Sigma Chemical Co. St. Louis, MO.
Preparation of Hapten-Modified Cells
Erythrocyte-free (treated with .83% Tris/NH4C1)
spleen cells (1 X 107/ml) were mixed 1:1 (volume:volume) with 10 mM TNBS for 8-10 min at room temperature. Following incubation, cells were washed 3X
with HBSS, counted, and resuspended at the appropriate concentration for use.
Anterior Chamber Inoculations
Cells were delivered to the anterior chamber in
0.005 ml volume using a Hamilton Microliter syringe
(Hamilton Co., Reno, NV) fitted with a 33 G needle.
Mice were lightly anesthetized with Metofane (methoxyflurane; Pitman-Moore, Mundelein, IL) and injections were done under a dissecting microscope. Anterior chamber injection was done 1-24 hr prior to
immunization. For TNP-spl, 5 X 105 cells and for
primed T cells, 1 X 105 cells were injected in .005 ml.
In Vivo Assays
CHS to TNP: Mice were injected subcutaneously
with 0.2 ml of a 10 mM solution of TNBS in phosphate buffered saline (PBS). Seven days later, animals
were ear challenged with 0.1% 2,4,6-trinitrochlorobenzene (TNCB) in acetone/olive oil (3:1). The right
ear received 0.015 ml of TNCB, while the left ear was
unchallenged. Values are expressed as units of swelling with one unit = 10~3 cm. Background values obtained from challenged, naive mice were subtracted
from each group.
DTH to proteins: Animals were injected subcutaneously with 100 /tig of protein in 0.1 ml of PBS mixed
with .1 ml of 10 mg/ml A1(OH)3 and 10 mg/ml
Mg(OH)2. Seven days later, mice were challenged in
the right footpad with 0.033 ml antigen in PBS. The
left footpad received 0.033 ml of PBS. Values are expressed in units of swelling with one unit = 10"3 cm.
Background values obtained from challenged, naive
mice were subtracted from each group.
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INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE / April 1992
Immunization for Primed T Cells:
Primed T cells were obtained from the spleen and
draining lymph nodes of immune mice. Mice were
injected subcutaneously with 100 jug of antigen in 0.1
ml PBS emulsified 1:1 with complete Freund's adjuvant (Sigma). Ten to fourteen days later spleen and
draining lymph nodes were removed, single cell suspensions prepared, and T cells purified.
Purification of T Cells:
T cells were prepared from single cell suspensions
of erythrocyte free spleens and lymph nodes2. Five
milliliter Econo columns (BioRad, Richmond, CA)
were filled with glass beads (mean diameter = 0.2
mm) coated with normal mouse immunoglobulin,
followed by the addition of a 1/5 dilution of rabbit
antimouse immunoglobulin. After 1 hr of incubation,
columns were washed 3X with HBSS, and cell suspensions were added at a concentration of 2 X 108 cells
per column (add 2 ml of 108/ml). The flow rate was
adjusted to 1 drop per 6-10 sec and cells were collected as they emerged from the column. Yield was
typically 25-30% of added cells that were >98% T
cells.
Statistical Analysis
Significant group differences were evaluated using
Student's t-test at P < 0.05.
Results
Amount of Light for Suppression
To better understand the mechanisms by which
light effects suppressed CHS, we sought to determine
REDUCTION
in Light Energy
the properties of light. In our previous report,3 we determined that only visible light was responsible for the
observed effects. Therefore, we focused our attention
on visible wavelengths. Because it was not possible to
get high amounts of light (eg, room light levels)
through all wavelength filters, it was necessary to determine the minimum level of light needed to standardize our experiments. Initially, we determined the
amount of light required to induce suppression of
CHS to TNP (TNP-ACAID).
The apparatus described in Materials and Methods
was fitted with neutral density filters. These filters allow precise reductions in the amount of light without
eliminating wavelengths in the visible range. The
starting point for these studies was 20 lux. Because we
had no a priori reason to know an appropriate starting
point, we measured the amount of light received by
the bottom shelf on the mouse cage rack in the
shadow cast by the shelf immediately above. Many
studies1"5 in our laboratories had demonstrated that
our experiments work if the mice are placed in this
position. (As a point of reference, the top shelf, which
is about 2-3 ft from the light source, receives 600-800
lux). Balb/cByJ mice were injected in the anterior
chamber with TNP-spl and placed in boxesfittedwith
neutral density filters that reduce light by 10%, 20%,
50%, 90%, and 99%. Twenty-four hours later, they
were immunized with TNBS and maintained in the
boxes for the remainder of the experiment. Six days
later, the animals were challenged with TNCB and
CHS that was measured 24 hr later. The data in Figure 1 show that a 99% reduction (0.2 lux) in light is
required to abolish suppression, while a 90% reduction (2 lux) did not. The remainder of the experiments
in this report were performed with light at 2 lux.
Contact Hypersensitivity
To TNCB (Balb/cByJ)
(Immune Control)
UNITS (cm x 1 0 " ° )
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Vol. 33
Fig. 1. Amount of light
for suppression. Balb/cByJ
mice were AC-injected with
TNP-T cells and immediately placed in boxes fitted
with neutral density filters
that reduce light from 0%99%. Twenty-four hours
later the mice were immunized with 0.2 ml of 10 mM
TNBS SC, and 5 days later
ear-challenged with TNCB.
Ear thickness was measured
24 hr later. Values are expressed as units of CHS with
1 unit = 10~3 cm (* denotes
significant suppression vs.
immune control).
No. 5
1791
LIGHT REGULATION OF ACAID / Ferguson er al
Contact Hypersensitivity
To TNCB (Balb/cByJ)
LIGHT
(Immune Control)
Fig. 2. Color of light necessary for suppression. Balb/cByJ mice were AC-injected with
TNP-T cells and immediately placed in boxes
fitted with Wratten filters for red, blue, and
green light. Twenty-four hours later the mice
were immunized with 0.2 ml of 10 mM TNBS
SC, and 5 days later ear-challenged with
TNCB. Ear thickness was measured 24 hr
later. Values are expressed as units of CHS
with 1 unit = 10~3 cm (* denotes significant
suppression vs. immune control).
UNITS (cm x 10~ 3 )
Determination of the Wavelength for Suppression
All molecules absorb light at specific wavelengths
and have a characteristic action spectrum.10 Therefore, to begin identifying the action spectrum of molecules that mediate the effect of light on the ocular
immune response, we used Wratten filters, photographic filters that pass light based on color. The experiment in Figure 2 shows that when Wratten filters
for red, blue, and green light are used, only green light
supports the development of suppressed CHS.
Because the green filter lets light pass at multiple
wavelengths, we purchased narrow bandfilters,fitted
the apparatus with them, and repeated the experiment in Figure 2. Filters from 400-460 nm and 530750 nm were uniformly negative, ie, no suppressed
CHS was seen (data not shown). The most interesting
points were 510 and 500 nm, as shown in Figure 3.
Light at 510 and 500 nm support suppression, demonstrating that light near these wavelengths was responsible for the induction of TNP-ACAID. These wavelengths are two of the principle wavelengths in green
light.
Role of the Retina
The experiment in Figure 3 demonstrates that the
wavelengths responsible for suppression are near
500-510 nm. These wavelengths are very near the optimal absorption of several photopigments in the eye.
Ocular pigments in the human eye absorb maximally
at 496 nm (rod rhodopsin), 419 nm (blue cones), 531
nm (green cones), and 558 nm (red cones).10 Rodent
Wavelength
of
Light
Fig. 3. Determination of the wavelength for
suppression in Balb/cByJ mice. Balb/cByJ
mice were AC-injected with TNP-T cells and
immediately placed in boxes fitted with
narrow-band wavelength filters. Twenty-four
hours later the mice were immunized with 0.2
ml of 10 mM TNBS SC, and 5 days later earchallenged with TNCB. Ear thickness was
measured 24 hr later. Values are expressed as
units of CHS with 1 unit = 10"3 cm (* denotes
significant suppression vs. immune control).
Visible
Contact Hypersensitivity
To TNCB (Balb/ByJ)
(Immune Control)
^Hl
Visible
H ^^
490 nm
H |
500 nm
^ ^ H^
510 nm
^^M
520 nm
^^H
' *
—
'
*
UNITS ( c m x 10"
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INVESTIGATIVE OPHTHALMOLOGY b VISUAL SCIENCE / April 1992
pigments are very similar, and evidence exists for another pigment very near the absorption spectrum of
rhodopsin." Because these pigments are located in
the photoreceptors of the mammalian retina, we took
advantage of the availability of C3H/HeJ rd/rd mice.
These animals have severe degeneration of photoreceptors by 4 wk of age, and a total degeneration of
rods by 26 wk.1213 In several experiments we determined that 4-6-wk-old C3H/HEJ mice and 26-30wk-old C3H/HEJ mice displayed the same light/dark
effect as Balb/c mice (data not shown). Therefore, we
did the experiment in Figure 4 with 8-10-wk-old
C3H/HeJ mice. These data show that the same wavelength requirement existed for C3H/HEJ rd/rd and
Balb/c mice.
Extension of Light/Dark to Protein Antigens
The photoreactivity of TNP is a potential problem
that's encountered when the role of light in the suppression of CHS after anterior chamber injection of
TNP-spl is being assessed. Therefore, we determined
whether the effect of light could be extended to other
antigen systems. We have been unable to induce suppressed DTH to protein antigens by injecting soluble
protein into the anterior chamber. However, we have
determined (data not shown) that antigen specific
suppression can be induced by including a small number of antigen primed T cells in the anterior chamber
inoculum with small amounts of the immunizing
protein. As little as 1.5 y% of HEL can be included
with 1 X 105 HEL primed T cells to induce potent
suppression of DTH. Therefore, an experiment was
done using HEL and HEL primed T cells in C3H/HeJ
mice. The data in Figure 5 demonstrate that suppression of DTH to HEL was supported by light at 500
Wavelength
of
Contact Hypersensitivity
Light
To TNCB (C3H-rd/rd)
and 510 nm, as was suppression to TNP. The injection of 1 X 105 T cells plus 1.5 /ug of HEL intravenously, intraperitoneally, or subcutaneously has no
effect on immunity to HEL (data not shown).
Role of the Pineal Gland
Recent studies have suggested the pineal gland is a
light-sensitive organ.14 Therefore, we considered the
role of this organ in the light/dark effect in the eye.
This organ produces important compounds such as
melatonin and responds to circadian influences controlled by light. To test the role of the pineal gland, we
purchased neonatally pinealectomized (pinlx) mice.
These mice and sham pinealectomized controls were
injected in the anterior chamber with TNP-spl, immunized 24 hr later, and tested for CHS 6 d later by ear
challenge. After the experiment, the animals were examined surgically for successful pinealectomy. The
results in Figure 6 show that pinealectomized and
sham operated mice display suppressed CHS.
The Effect of Light on Immunity
Throughout the experiments in this report, we have
been determining the effect of various wavelengths of
light on ACAID. Our previous studies demonstrated
that ACAID is initiated by an intraocular T cell reaction1 -2A that is influenced by visible light.3 We already
have shown that dark rearing animals and placing
light-reared animals in the dark post immunization
has no effect on intravenously induced tolerance of
CHS responses.3 However, a question arose regarding
the effect of the various wavelengths of light on systemic immunity. To address this question, we per-
(Immune Control)
UNITS (cm x 10~°)
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Vol. 33
Fig. 4. Determination of the wavelength for
suppression in C3H/HeJ mice—role of the retina. C3H/HeJ mice were AC-injected with
TNP-T cells and immediately placed in boxes
fitted with narrow band wavelength filters.
Twenty-four hours later the mice were immunized with 0.2 ml of 10 mM TNBS SC, and 5
days later ear-challenged with TNCB. Ear
thickness was measured 24 hr later. Values are
expressed as units of CHS with 1 unit = 10~3
cm (* denotes significant suppression vs. immune control).
No. 5
LIGHT REGULATION OF ACAID / Ferguson er ol
Fig. 5. Extension of light/dark to
protein antigens. C3H/HeJ mice were
AC-injected with 1 X 105 HEL primed
T cells and 1.5 ^g HEL, and immediately placed in boxesfittedwith narrow
band wavelength filters. Twenty-four
hours later mice were immunized SC
with 100 fig HEL in Maalox. Seven
days later mice were challenged in the
right footpad with 0.033 ml HEL in
PBS; the left footpad received 0.033 ml
of PBS. Values are expressed in units of
footpad swelling, with one unit = 10~3
cm (* denotes significant suppression
vs. immune control).
Wavelength
of
Light
1793
Delayed-Type Hypersensitivity
To HEL (C3H/HeJ)
(Immune Control)
UNITS (cm x 1 0 " ° )
organ,14 does not appear to play a role because pinealectomized mice display suppressed CHS.
The results presented here show that the effect of
light on ocular immune responses extends beyond the
TNP-ACAID system. The suppression of DTH after
anterior chamber injection of HEL and T cells also
depends on light at 500-510 nm. HEL absorbs light in
the UV range (280 nm) as do most other protein antigens. In addition, we also have extended our observations to the von Szily model of experimental retinal
necrosis.6 The contralateral retinitis observed after
the anterior chamber injection of HSV-1 depends on
visible light. When animals are dark reared, retinal
necrosis is not observed in the ipsilateral or contralateral eye.5 Whether this is governed by 500-510 nm
light remains to be determined.
The effect of UV light on immunity is well studied,15 but little is known about the effect of visible
formed the experiments in Figure 7. Mice were immunized for CHS (Fig 7 A) or DTH (Fig 7B) and placed in
the various lighting conditions. These results demonstrate that the wavelengths of light that influence
ACAID have no effect on systemic immunity.
Discussion
The results presented in this report extend our previous observations concerning the effect of visible
light on the ocular immune response. We show that
suppressed CHS after anterior chamber injection of
antigen is governed by green light in the 500-510 nm
range. Although these wavelengths are near the absorption of rhodopsin,10 the effect of light apparently
is not governed by detectable retinal pigments. This is
because the same wavelengths supported suppression
in C3H/HEJ rd/rd mice, which are devoid of photoreceptors. In addition, the pineal gland, a light-sensitive
Contact Hypersensitivity
To TNCB (Balb/cTac)
AC Pinlx
Fig. 6. Role of the pineal gland. Pinealectomized (Pinlx) or sham-pinealectomized Balb/
cTac mice were AC injected with TNP-T cells.
Twenty-four hours later the mice were immunized with 0.2 ml of 10 mM TNBS SC, and 5
days later ear-challenged with TNCB. Ear
thickness was measured 24 hr later. Values are
expressed as units of CHS with 1 unit = 10~3
cm (* denotes significant suppression vs. immune control).
No
No
Yes
No
No
Yes
Yes
Yes
^
—
i
*
UNITS (cm x 1 0 ~ 3 )
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INVESTIGATIVE OPHTHALMOLOGY 6 VISUAL SCIENCE / April 1992
Vol. 33
A. CHS to TNCB
Wavelength
of
Light
Contact Hypersensitivity
UNITS (cm x
B. DTH to HEL
Wavelength
of
Light
Delayed-Type Hypersensitivity
Fig. 7. Effect of light on immunity. (A)
Balbc/ByJ mice were immunized with 0.2 ml
of 10 mM TNBS and placed in the boxes fitted
with the narrow-band wavelengthfilters.Five
days later ears were challenged with TNCB,
and ear thickness measured 24 hr later. Values
are expressed as units of CHS with 1 unit
= 10"3 cm. (B) C3H/HeJ mice were immunized SC with 100 /ig HEL in Maalox and
placed in the boxes fitted with the narrow
band wavelengthfilters.Seven days later mice
were challenged in the right footpad with
0.033 ml HEL in PBS; the left footpad received 0.033 ml of PBS. Values are expressed
in units of footpad swelling, with one unit
= 10~3cm.
UNITS (cm x .ID""0)
light on immune responses. To our knowledge, there
is virtually no literature that documents an effect of
visible light directly on in vivo immune responses.
Studies have been performed that show an effect of
visible light on cultured cells, such as Chinese hamster
ovary cells.16"20 These effects have been attributed to
the photochemical interaction between fluorescent
light and media components such asriboflavin,tryptophan, tyrosine, and HEPES buffer. This interaction
can lead to the formation of lipid peroxidases, superoxide anion, and H2O2, which inhibit or kill cultured
cells.19-20 Some studies have attempted to document a
direct interaction between visible light and DNA. It
has been shown that visible light can cause single
strand breaks in the DNA.20
One recent study documented the effect of constant
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darkness on autoimmunity to type II collagen.21
These results were attributed to circadian effects and
melatonin synthesis by the pineal gland. The results
of our previous study3 suggest that circadian influences may not be directly involved in his system and
the present study argues against a role for the pineal
gland.
While the effects of visible light on the immune
response have not been studied, the interactions between light and the eye have been studied extensively.
The eye absorbs light through its system of visual pigments located in the retina. These pigments include
the well known rod pigment rhodopsin and three
cone pigments: blue, green, and red. The maximum
absorption for these pigments in humans are: rhodopsin, 496 nm; blue cone, 419 nm; green cone, 531 nm;
LIGHT REGULATION OF ACAID / Ferguson er ol
No. 5
and red cone, 558 nm. Retinal rod pigments are more
abundant, stable, and better characterized than retinal cone pigments. The photoisomerization of photopigments starts a complex series of chemical reactions
and the initiation of the visual cycle. The initial isomerization of the photopigment is the only reaction
in vision that involves light.10 The remainder of the
reactions are non-light dependent and result in the
production of many products and intermediates that
may potentially affect immune reactions in the eye.
Unfortunately, our experiments with rd/rd mice may
rule out a role for the retina. However, the presence of
photopigment in other ocular structures, such as the
iris, has not been ruled out. Amphibians have been
shown to have rhodopsin localized in the iris.22 Also,
although retinal pigments absorb maximally at the
above wavelengths, they also have absorption at other
visible wavelengths and in the UV range. Even the
possibility that T cells included in the anterior
chamber inoculum have 500-510 nm absorbing pigments has to be considered.
Adult rd/rd mice are devoid of photoreceptors.
However, they do retain a normal ganglion cell layer,
retinal pigment epithelium, and Miiller cells. Although these layers are intact and may inhibit immune function (eg, Miiller cells23), they do not result
in a light-induced neuronal signal. This is solely a
property of the photoreceptors in the neurosensory
retina. Our results seem to rule out the possibility that
visual phototransduction through the neurosensory
retina is responsible for the observed effect of green
light because rd/rd mice have no photoreceptors and
thus no phototransduction.
It is interesting that the effect of light on intraocular
immune reactions is confined to such a narrow range.
Further study will be required to evaluate the limited
wavelength requirements. The molecular mediator
(or mediators) for the light-induced effects on the immune response and the eye is not known, so further
study on the wavelength of light responsible for the
production of neurotransmitters (dopamine, serotonin, melatonin, histamine) and neuropeptides (vasointestinal peptide, substance P) may provide clues
to the role of light in ocular immunoregulation.
Key words: light, anterior chamber associated immune deviation, delayed-type hypersensitivity, immunoregulation,
Tcell
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