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How much sun? sunscreen?
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| Hi there
This is the first year I have to deal with psoriasis, My derm had me
use clobex for a month, which has cleared most of the redness. Its
starting to come back, and I understand the sun supposed to help.
What is reccomended sunshine wise? Short periods, long periods? How
about sunscreen? Does that stop the sun's benefits?
any pointers appreciated
Thanks kindly
Liam
| |
|
| Hi Liam-
Wow! There are so many variables, it might be hard to give a
definitive answer to your questions. I've been battling P for about 2
years, and the only thing that helps is the sun. I'm a mess in the
winter, but when the warmer weather hits and I can be outside, wear
shorts, go shirtless, etc., I get clearer. I go for 15-20 minute
exposures daily or every other day, per my derm's recommendations. I
started out at 10 minutes until I got a little tan going. If I'm going
to be in the sun for extended periods of time, like doing yard work,
outdoor activities, etc., I try to be careful not to get sunburned, as
this can make P worse.
Some things you might want to consider:
1) type of P you have
2) your skin type and sensitivity to the sun (I have a fairly light
complexion but tan easily)
3) altitude - you need less exposure time at higher altitudes. Also,
the amount of air pollution in your area might be a consideration
4) any medications (prescription or OTC) you are taking or using
topically that might increase your sensitivity to UV rays
5) any history of skin cancer, melanoma, etc in yourself or family
members.
I'm sure there are other things to think about, but maybe this is a
start. Probably best advice would be to be careful about sun exposure,
not over-do it, and follow your derm's advice.
Hope this helps some.
Peace,
Gary
| |
| JXStern 2006-04-17, 11:19 am |
| On 16 Apr 2006 11:37:36 -0700, "Liam" <wallydiver_19@hotmail.com>
wrote:
>Hi there
>
>This is the first year I have to deal with psoriasis, My derm had me
>use clobex for a month, which has cleared most of the redness. Its
>starting to come back, and I understand the sun supposed to help.
>What is reccomended sunshine wise? Short periods, long periods? How
>about sunscreen? Does that stop the sun's benefits?
>any pointers appreciated
>Thanks kindly
>Liam
In general, what you want from the sun are the UV rays, the ones which
tan and burn you, and which the sunscreens block. So if you're going
to be out there for hours, you might still use sunscreen, but if
you're going out to get some sun specifically for the psoriasis, you
probably want no screens at all. Though a little baby oil or
something to moisterize is good, just make sure it does NOT have any
sunscreen ingredients!
When you get a medical office UV treatment they take you up to the
point of burning. I do not recommend that for sun treatment. Keep it
modest, whatever you would normally do, just be a little more diligent
about it, and see if that helps.
Note that sunlight/UV does not work for everyone, for some people it
is an active irritant.
I find it does help me, even a few minutes a day is noticeably better
than none, at least a few days a week is good, everyday is better as
my schedule, and weather, allows.
Geography matters, too. You get UVB only when the sun is nearly
overhead, and you don't get much of anything when the sun is low on
the horizon. So if you're at extreme northern or southern latitudes,
it's just plain hard to get a lot of effective sun. And altitude -
over five thousand feet you get UV a lot faster, and over ten thousand
feet even more seriously faster! But if you're at those altitudes,
you probably know about it already.
When the sun don't shine, I've also used commercial tanning salons,
going for modest exposures.
Oh yeah, one more variable is your skin type, if you're light-skinned,
in general keep the exposures down, if you're dark-skinned, you
probably want a bit more, certainly you can take a bit more!
Experiment, start slow, and see what happens!
Best wishes,
J.
| |
|
| just some random thoughts..
all good answers but not quite accurate...uvb is what you want ..they
are what cause the burning so limit your exposure to one half hour in
direct sun..after that use a sunscsreen. You do not want to tan which
comes from uva.... a tan limits uvb's getting through to produce
vitamin D (actually a hormone) .It is the vitamin D which effects the
status of your Psoriasis. It takes about 2 wks to a month for a
positive change by changing you learned immuned response.You have to
wait for your old misprogrammed(by dendritic cells) t-cells to
die(their lifespan is about a month or less).. and new vitamin D
production (which is a steroid and must go through a few steps (altered
by the liver and kidney) before its an active form to effect the new
dendritic t cell's by blocking their receptors and ending the symptoms
of P.
This is why, P worsens over winter ......with no sun and as stored
Vitamin D in the tissues diminishes, the receptors on the new dendritic
cells are not blocked by the D and the cells receptors attach to
proteins bits from the environment and are perceived as a threat via a
faulty learned immune response..this is why some foods seem to increase
the P. They (dendritic cells) send chemical messages to the t-cells to
attacking areas of the body which are ..resulting in plaques etc...As
you get older, your Vitamin D production decreases and hence, older
people almost always have increased P.
You can make 20,000 units of Vitamin D from cholesterol in your skin in
about 20 minutes..after that is starts to break down so you gain little
after 20 minutes and then uv can harm you skin. So, after 20 minutes,
slap on the sunscreen. As common sense dictates, darker skinned people
need longer time and your latitude and time of year are factors to
consider.
In the winter...people travel to the sun, not for warmth...it's for the
vitamin D they're lacking
| |
| randall 2006-04-20, 1:19 am |
|
bj wrote:
> just some random thoughts..
>
> all good answers but not quite accurate...uvb is what you want ..they
> are what cause the burning, so limit your exposure to one half hour in
> direct sun..after that use a sunscsreen. You do not want to tan which
> comes from uva.... a tan limits uvb's getting through to produce
> vitamin D (actually a hormone) .It is the vitamin D which effects the
> status of your Psoriasis. It takes about 2 wks to a month for a
> positive change by changing you learned immuned response.You have to
> wait for your old misprogrammed (by dendritic cells) t-cells to
> die (their lifespan is about a month or less).. and new vitamin D
> production (which is a steroid and must go through a few steps (altered
> by the liver and kidney) before its an active form to effect the new
> dendritic t cell's by blocking their receptors and ending the symptoms
> of P.
>
> This is why, P worsens over winter ......with no sun and as stored
> Vitamin D in the tissues diminishes, the receptors on the new dendritic
> cells are not blocked by the D and the cells receptors attach to
> proteins bits from the environment and are perceived as a threat via a
> faulty learned immune response..this is why some foods seem to increase
> the P. They (dendritic cells) send chemical messages to the t-cells to
> attacking areas of the body which are ..resulting in plaques etc...As
> you get older, your Vitamin D production decreases and hence, older
> people almost always have increased P.
>
> You can make 20,000 units of Vitamin D from cholesterol in your skin in
> about 20 minutes..after that is starts to break down so you gain little
> after 20 minutes and then uv can harm you skin. So, after 20 minutes,
> slap on the sunscreen. As common sense dictates, darker skinned people
> need longer time and your latitude and time of year are factors to
> consider.
>
> In the winter...people travel to the sun, not for warmth...it's for the
> vitamin D they're lacking
Hi bj,
Haven't seen your around in awhile. You were clearing nicely when you
last disaPPeared. You had stoPPed treatments at the time iirc.
Great answer btw.
Let's shed some light on D3.
http://www.biocarta.com/pathfiles/m_vdrPathway.asp
UVB slows rantes.
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D16284793
Effects of ultraviolet B irradiation on the production of regulated
upon activation normal T-cell expressed and secreted protein in
cultured human epidermal keratinocytes.
Arakawa S, Hatano Y, Katagiri K, Terashi H, Fujiwara S.
Department of Anatomy, Biology and Medicine (Dermatology), Faculty of
Medicine, Oita University, Oita, Japan, arakawa@med.oita-u.ac.jp.
The modulatory effects of ultraviolet B (UVB) irradiation on cutaneous
inflammatory responses are well known but their mechanism remains
obscure. It has been proposed that regulated upon activation normal
T-cell expressed and secreted protein (RANTES), which is one of the
chemokines produced by epidermal keratinocytes, might play an important
role in the pathogenesis of cutaneous inflammatory disorders, such as
atopic dermatitis and psoriasis vulgaris. This study was designed to
determine whether UVB irradiation could affect the production of RANTES
that is induced in cultured normal human epidermal keratinocytes upon
stimulation by inflammatory cytokines. We measured levels of the
transcript of the gene for RANTES in cultured keratinocytes and of
RANTES itself in culture supernatants by semiquantitative reverse
transcription and the polymerase chain reaction and by an enzyme-linked
immunosorbant assay (ELISA), respectively. Neither the transcript nor
RANTES itself was detected without prior stimulation of cells by tumor
necrosis factor alpha (TNF-alpha) and/or interferon gamma (IFN-gamma)
and production of RANTES was not induced by UVB (100 J/m(2))
irradiation alone. Cells were irradiated with UVB just before addition
of TNF-alpha and IFN-gamma to the medium and then cells and culture
supernatants were harvested 12, 24, and 36 h later. In both irradiated
and non-irradiated cells, RANTES mRNA was first detected at 12 h and
the level increased subsequently. RANTES itself was detected at 24 h,
with a higher level at 36 h. At all time points examined, UVB
irradiation inhibited the production of RANTES mRNA and of the protein
itself. These results suggest that suppression of the production of
RANTES by epidermal keratinocytes might be involved in the modulatory
effects of UVB irradiation on cutaneous inflammation.
PMID: 16284793
How about a randall rant on rantes?
Sure!
http://www.ncbi.nlm.nih.gov/entrez/...pmax=3D100&ter=
m=3Drantes+psoriasis
&
http://www.ncbi.nlm.nih.gov/entrez/...pmax=3D100&ter=
m=3Dil-8+psoriasis
&
http://groups.google.com/groups/sea...s&qt_s=3DSearch
&
http://groups.google.com/groups/sea...sis&qt_s=3DSea=
rch
http://www.ncbi.nlm.nih.gov/entrez/...cgi?id=3D601267
*601267 Links
CHEMOKINE, CC MOTIF, RECEPTOR 2; CCR2
Alternative titles; symbols
CMKBR2
CKR2
MONOCYTE CHEMOTACTIC PROTEIN 1 RECEPTOR
MCP1 RECEPTOR
CCR2A, INCLUDED; CKR2A, INCLUDED
CCR2B, INCLUDED; CKR2B, INCLUDED
Gene map locus 3p21
TEXT
MCP1, or monocyte chemoattractant protein (158105), is produced by
endothelial cells, smooth muscle cells, and macrophages in response to
a variety of mediators. It may be involved in inflammatory processes in
disorders including rheumatoid arthritis, alveolitis, and tumor
infiltration. It may also be an important component of monocyte
invasion of artery walls in atherosclerosis (Charo et al. (1994))
<sniP>
----------------------------------------------------------------
http://www.ncbi.nlm.nih.gov/entrez/...DRetrieve&dopt=
=3DGraphics&list_uids=3D1231
------------------------------------------------------------
http://www.ncbi.nlm.nih.gov/entrez/...db=3DPubMed&li=
st_uids=3D15370700&dopt=3DAbstract
Expression of CCR2 on monocytes and macrophages in chronically
inflamed skin in atopic dermatitis and psoriasis.
Vestergaard C, Just H, Baumgartner Nielsen J, Thestrup-Pedersen K,
Deleuran M.
Department of Dermatology, Marselisborg Centret, Aarhus County
Hospital, university of Aarhus, Aarhus, Denmark. Chr-vest@post9.tele.dk
Monocytes form a significant component of the inflammatory reaction
taking place in the skin of atopic dermatitis and psoriasis. Chemokines
are pivotal in mediating the attraction of leucocytes to sites of
inflammation. The CC-chemokine, monocyte chemotactic protein 1
(MCP-1/CCL2), is expressed by keratinocytes in both atopic dermatitis
and psoriasis. MCP-1 binds to the chemokine receptor CCR2 which is
known to be expressed on monocytes and macrophages. We examined the
expression of CCR2 on peripheral blood monocytes from patients with
psoriasis (n=3D8) and atopic dermatitis (n=3D7) and found it to be
expressed on approximately 90% of the cells, whereas monocytes from
healthy donors had a significantly lower CCR2 expression (p<0.05). Skin
biopsies from patients suffering from atopic dermatitis and psoriasis
revealed that CCR2-positive cells expressed CD163, a marker for
monocytes/macrophages. However, not all CD163-positive cells expressed
CCR2, which could be interpreted as a mechanism for retaining the
macrophages in the skin. Furthermore, we found that keratinocytes are
able to express MCP-1, when stimulated with tumour necrosis
factor-alpha and/or interferon-gamma in a dose-dependent manner. Thus
MCP-1 and CCR2 interaction is likely of importance for the
monocyte/macrophage trafficking of inflammatory skin disorders.
PMID: 15370700
CD56brightCD16(-) NK cells accumulate in psoriatic skin in response to
CXCL10 and CCL5 and exacerbate skin inflammation.
Ottaviani C, Nasorri F, Bedini C, de Pita O, Girolomoni G, Cavani A.
Laboratory of Immunology and Allergology, Istituto Dermopatico
dell'Immacolata, IRCCS, Rome, Italy.
Psoriasis is an immune-mediated skin disease characterized by
lymphocytic infiltration and altered keratinocyte differentiation.
Using immunohistochemical techniques we found that the cellular
infiltrate in acute psoriatic plaques includes 5-8% CD3(-)CD56(+)
natural killer (NK) cells, mostly localized in the mid and papillary
dermis. NK lymphocytes isolated from punch biopsy specimens of
psoriatic plaques showed a CD56(bright)CD16(-)CD158b(-) phenotype,
failed to express the skin homing cutaneous lymphocyte-associated
antigen and released abundant IFN-gamma upon stimulation. Supernatants
from psoriatic NK cells induced MHC class II and ICAM-1 expression and
release of CXCL10 and CCL5 by cultured psoriatic keratinocytes. Skin NK
cells expressed high levels of the chemokines receptors CXCR3 and CCR5,
intermediate amounts of CXCR1, CCR6 and CCR8, and low levels of CCR1,
CCR2, CCR4, CCR7 and CX3CR1. In addition, they promptly migrated in
vitro toward CXCL10, CCL5, supernatants of IFN-gamma-activated
psoriatic keratinocytes and, to a lower extent, CCL20 and CCL4. In
contrast, they failed to migrate toward CXCL8, CCL1, CCL2, CCL3, CCL17,
CCL19 and CX3CL1. Taken together, our results implicate NK lymphocytes
as newly identified protagonists in the pathogenesis of psoriasis.
Their distinctive homing properties should be taken into account in the
design of specific therapy aimed at blocking pathogenic cell
accumulation in the skin.
PMID: 16323244
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D10843722
&
CCR2 =3D Mcp1, so,
http://www.ncbi.nlm.nih.gov/entrez/...pmax=3D100&ter=
m=3Dmcp1+psoriasis
The lps, il-10 sin?
http://www.biocarta.com/pathfiles/h_il10Pathway.asp
For the coup de gr=E2ce, the il-22 crohn's connections.
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D16537974
IL-22 is increased in active Crohn's disease and promotes
proinflammatory gene expression and intestinal epithelial cell
migration.
Brand S, Beigel F, Olszak T, Zitzmann K, Eichhorst ST, Otte JM,
Diepolder H, Marquardt A, Jagla W, Popp A, Leclair S, Herrmann K,
Seiderer J, Ochsenkuhn T, Goke B, Auernhammer CJ, Dambacher J.
Department of Medicine II, University-Hospital Munich-Grosshadern,
University of Munich, Germany. stephan.brand@med.uni-muenchen.de
IL-22 is produced by activated T cells and signals through a receptor
complex consisting of IL-22R1 and IL-10R2. The aim of this study was to
analyze IL-22 receptor expression, signal transduction, and specific
biological functions of this cytokine system in intestinal epithelial
cells (IEC). Expression studies were performed by RT-PCR. Signal
transduction was analyzed by Western blot experiments, cell
proliferation by
3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2=
H-tetrazolium
assay and Fas-induced apoptosis by flow cytometry. IEC migration was
studied in wounding assays. The IEC lines Caco-2, DLD-1, SW480, HCT116,
and HT-29 express both IL-22 receptor subunits IL-22R1 and IL-10R2.
Stimulation with TNF-alpha, IL-1beta, and LPS significantly upregulated
IL-22R1 without affecting IL-10R2 mRNA expression. IL-22 binding to its
receptor complex activates STAT1/3, Akt, ERK1/2, and SAPK/JNK MAP
kinases. IL-22 significantly increased cell proliferation (P =3D 0.002)
and phosphatidylinsitol 3-kinase-dependent IEC cell migration (P <
0=2E00001) as well as mRNA expression of TNF-alpha, IL-8, and human
beta-defensin-2. IL-22 had no effect on Fas-induced apoptosis. IL-22
mRNA expression was increased in inflamed colonic lesions of patients
with Crohn's disease and correlated highly with the IL-8 expression in
these lesions (r =3D 0.840). Moreover, IL-22 expression was increased in
murine dextran sulfate sodium-induced colitis. IEC express functional
receptors for IL-22, which increases the expression of proinflammatory
cytokines and promotes the innate immune response by increased defensin
expression. Moreover, our data indicate intestinal barrier functions
for this cytokine-promoting IEC migration, which suggests an important
function in intestinal inflammation and wound healing. IL-22 is
increased in active Crohn's disease and promotes proinflammatory gene
expression and IEC migration.
PMID: 16537974
And back to psoriasis,
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D16619290
IL-22 regulates the expression of genes responsible for antimicrobial
defense, cellular differentiation, and mobility in keratinocytes: a
potential role in psoriasis.
Wolk K, Witte E, Wallace E, Docke WD, Kunz S, Asadullah K, Volk HD,
Sterry W, Sabat R.
Interdisciplinary Group of Molecular Immunopathology,
Dermatology/Medical Immunology, university Hospital Charite, Berlin,
Germany.
IL-22 is an IFN-IL-10 cytokine family member, which is produced by
activated Th1 and NK cells and acts primarily on epithelial cells. Here
we demonstrate that IL-22, in contrast to its relative IFN-gamma,
regulates the expression of only a few genes in keratinocytes. This is
due to varied signal transduction. Gene expressions regulated by IL-22
should enhance antimicrobial defense [psoriasin (S100A7), calgranulin A
(S100A8), calgranulin B (S100A9)], inhibit cellular differentiation
(e.g., profilaggrin, keratins 1 and 10, kallikrein 7), and increase
cellular mobility [e.g., matrix metalloproteinease 1 (MMP1, collagenase
1), MMP3 (stromelysin 1), desmocollin 1]. In contrast, IFN-gamma
favored the expression of MHC pathway molecules, adhesion molecules,
cytokines, chemokines, and their receptors. The IL-22 effects were
transcriptional and either independent of protein synthesis and
secretion, or mediated by a secreted protein. Inflammatory conditions,
but not keratinocyte differentiation, amplified the IL-22 effects.
IL-22 application in mice enhanced cutaneous S100A9 and MMP1
expression. High IL-22 levels in psoriatic skin were associated with
strongly up-regulated cutaneous S100A7, S100A8, S100A9, and MMP1
expression. Psoriatic patients showed strongly elevated IL-22 plasma
levels, which correlated with the disease severity. Expression of IL-22
and IL-22-regulated genes was reduced by anti-psoriatic therapy. In
summary, despite similarities, IFN-gamma primarily amplifies
inflammation, while IL-22 may be important in the innate immunity and
reorganization of epithelia.
PMID: 16619290
And the IL-10 and P connect (note-IL-10 lowers the Th1 skew and slows
psoriasis)
http://www.ncbi.nlm.nih.gov/entrez/...db=3Dpubmed&do=
pt=3DAbstract&list_uids=3D16464746
Keratinocytes as targets for interleukin-10-related cytokines: a
putative role in the pathogenesis of psoriasis.
Boniface K, Lecron JC, Bernard FX, Dagregorio G, Guillet G, Nau F,
Morel F.
Laboratoire Cytokines et Inflammation, UPRES-EA 3806, CHU de Poitiers,
Universite de Poitiers, 40 Avenue du Recteur Pineau, 86022 Poitiers,
France.
Cytokines are key factors in the cross talk between the immune system
and other systems including hepatic, nervous, cardiac and cutaneous
systems, leading to an adaptive and integrated response of the organism
to stress. They are also involved in the regulation of many processes,
including hematopoiesis, the immune response and inflammation. IL-10 is
one of the most important anti-inflammatory cytokines. Five cytokines
structurally related to IL-10 have been described and presently form
this family of cytokines: IL-19, IL-20, IL-22, IL-24 and IL-26. In
contrast to IL-10, these cytokines display pro-inflammatory activities
in different tissues, including skin. Indeed, some of them induce an
inflammatory keratinocyte gene expression profile and an epidermis
histology resembling psoriatic lesions. In this review, we discuss
recent knowledge about the effects of cytokines of the IL-10 family on
keratinocytes and their potential role in psoriasis, a cutaneous
inflammatory disease.
PMID: 16464746
Regulation of T cells and cytokines by the interleukin-10
(IL-10)-family cytokines IL-19, IL-20, IL-22, IL-24 and IL-26.
Oral HB, Kotenko SV, Yilmaz M, Mani O, Zumkehr J, Blaser K, Akdis CA,
Akdis M.
Department of Microbiology & Infectious Diseases, Immunology Unit,
Uludag university School of Medicine, 16059 Bursa, Turkey.
oralb@uludag.edu.tr
The family of IL-10-related cytokines includes several human members,
IL-19, IL-20, IL-22, IL-24 and IL-26, and a series of herpesviral and
poxviral paralogs. Some of these cytokines share common receptor
subunits. In this study, we investigated the effects of these cytokines
on naive T cell differentiation, antigen-specific T cell suppression,
survival ad expression of surface markers in comparison to IL-10 and
cytomegalovirus (CMV)-IL-10. Human CD45RA(+) T cells were stimulated in
the presence of IL-10-family cytokines in sequential 12-day cycles.
After three to four cycles of stimulation, IL-10 and CMV-IL-10 led to
increased IFN-gamma and IL-10 but decreased IL-4 and IL-13.
Interestingly, long-term exposure of T cells to IL-19, IL-20 and IL-22
down-regulated IFN-gamma but up-regulated IL-4 and IL-13 in T cells and
supported the polarization of naive T cells to Th2-like cells. In
contrast, neutralization of endogenous IL-22 activity by IL-22-binding
protein decreased IL-4, IL-13 and IFN-gamma synthesis. The
antigen-specific suppressor activity of IL-10 and CMV-IL-10 was not
observed for any of the other IL-10-family cytokines. These data
demonstrate that IL-19, IL-20 and IL-22 may participate in T
cell-mediated diseases by distinct regulation of T cell cytokine
profiles.
PMID: 16365913
Bingo! ConA and CMV links to P via STAT3? Viral monkey bizness or what?
Hydrodynamic gene delivery of interleukin-22 protects the mouse liver
from concanavalin A-, carbon tetrachloride-, and Fas ligand-induced
injury via activation of STAT3.
Pan H, Hong F, Radaeva S, Gao B.
Section on Liver Biology, Laboratory of Physiologic Studies, National
Institute on Alcohol Abuse and Alcoholism, National Institutes of
Health, Bethesda, MD 20892, USA.
Interleukin-22 (IL-22) is a recently identified T cell-derived cytokine
whose biological significance remains obscure. Previously, we have
shown that IL-22 plays a protective role in T cell-mediated hepatitis
induced by Concanavalin A (Con A), acting as a survival factor for
hepatocytes. In the present paper, we demonstrate that hydrodynamic
gene delivery of IL-22 cDNA driven either by a liver-specific albumin
promoter or a human cytomegalovirus (CMV) promoter results in IL-22
protein expression, STAT3 activation, and expression of several
anti-apoptotic proteins, including Bcl-xL, Bcl-2, and Mcl-1 in the
liver. Immunohistochemical analysis reveals that IL-22 protein
expression is mainly detected in the cytoplasm of hepatocytes.
Overexpression of IL-22 by hydrodynamic gene delivery significantly
protects against liver injury, necrosis, and apoptosis induced by
administration of Con A, carbon tetrachloride (CCl4), or the Fas
agonist Jo-2 mAb. Western blot analyses show that overexpression of
IL-22 significantly enhances activation of STAT3 and expression of
Bcl-xL, Bcl-2, and Mcl-1 proteins in liver injury induced by Con A. In
conclusion, hydrodynamic gene delivery of IL-22 protects against liver
injury induced by a variety of toxins, suggesting the therapeutic
potential of IL-22 in treating human liver disease.
PMID: 16212920
Of all the gall, is your liver uP to this!
Cytokines, STATs and liver disease.
Gao B.
Section on Liver Biology, Laboratory of Physiologic Studies, National
Institute on Alcohol Abuse and Alcoholism, National Institutes of
Health, Bethesda, MD 20892, USA. bgao@mail.nih.gov
The Janus kinase-signal transducers and activators of transcription
(JAK-STAT) signaling pathway, activated by more than 50 cytokines or
growth factors, plays critical roles in a wide variety of cellular
functions in the hematopoietic, immune, neuronal and hepatic systems.
In the liver, this signaling pathway, activated by more than 20
cytokines, growth factors, hormones, and hepatitis viral proteins,
plays critical roles in antiviral defense, acute phase response,
hepatic injury, repair, inflammation, transformation, and hepatitis.
This article reviews the biological significance of STAT1, 2, 3, 4, 5,
6 in hepatic functions and diseases.
PMID: 16191414
The IL-10 P connection is bigger then this, more then likely?
http://www.ncbi.nlm.nih.gov/entrez/...cgi?id=3D124092
[=2E..]
IL10 is thought to play a key role in psoriasis (see 177900). Its
highly polymorphic promoter contains 2 informative microsatellites,
IL10.G and IL10.R. Asadullah et al. (2001) analyzed IL10 promoter
polymorphisms in 78 patients and 80 healthy controls. The distribution
of IL10.G and IL10.R microsatellite alleles did not vary between
patients and controls. In addition, when the psoriasis patients were
stratified according to age of onset (younger than 40, or 40 and
older), no difference in allele distribution was observed; however, a
clear differential distribution was revealed at the IL10.G locus when
patients were stratified according to whether they had a positive
family history of psoriasis (p =3D 0.04). This difference was due to an
overrepresentation of the IL10.G13 allele in those patients with
familial disease (40.4% vs 19.6%, chi square =3D 7.292, p =3D 0.007). The
positive association of allele IL10.G13 with familial psoriasis was
especially strong when patients with early onset were compared with
those with early onset against a nonfamilial background (39.6% vs
14.5%, chi square =3D 8.959, p =3D 0.003). Patients with age of onset of
less than 40 were 4-fold more likely to have a psoriatic family
background if they carried the IL10.G13 allele. These data suggested
that the IL10 locus contributes to the heritability of psoriasis
susceptibility.
<sniP>
I'm watching criminal minds. I wonder if I left out a susPect or three?
lol
randall...psoriasis genes go stat in the light of day!
| |
|
| thanks randall,
i had been clear for eight months and then went off the suppliments
again over the last three months...i noticed in full remission a could
eat anything (the dendritic cells receptors were blocked by the
D)...but as D3 levels dropped and my P returned , the nightshades etc
appeared to cause flareups....
i began the suppliments and sun again over the last month and am
clearing as before and should be completely clear by next month. This
last experiment involved uvb on only one leg,arm etc..one leg and arm
exposed and the other covered....it made no difference....both sides
cleared at the same rate.
| |
| JXStern 2006-04-20, 1:19 am |
| On 19 Apr 2006 14:29:50 -0700, "bj" <bjmacc@msn.com> wrote:
>This is why, P worsens over winter ......with no sun and as stored
>Vitamin D in the tissues diminishes, the receptors on the new dendritic
>cells are not blocked by the D and the cells receptors attach to
>proteins bits from the environment and are perceived as a threat via a
>faulty learned immune response..this is why some foods seem to increase
>the P. They (dendritic cells) send chemical messages to the t-cells to
>attacking areas of the body which are ..resulting in plaques etc...As
>you get older, your Vitamin D production decreases and hence, older
>people almost always have increased P.
>
>You can make 20,000 units of Vitamin D from cholesterol in your skin in
>about 20 minutes..after that is starts to break down so you gain little
>after 20 minutes and then uv can harm you skin. So, after 20 minutes,
>slap on the sunscreen. As common sense dictates, darker skinned people
>need longer time and your latitude and time of year are factors to
>consider.
>
>In the winter...people travel to the sun, not for warmth...it's for the
>vitamin D they're lacking
All good stuff, but if it were that simple, couldn't we just take a
little extra vitamin D and be happy?
Therapeutic UVB is usually intense for much shorter than 20 minutes, I
have no idea if that produces tons of vitamin D, or if more time at
less intensity would be better. The doctors seem to like to get you
on the edge of a burn, it doesn't seem to be a fixed-dose situation.
Again, if it were, they could just tell you to get some sun - at least
here in California, in the summer.
I've gotten as much benefit from UVA tanning salon or winter/morning
sun, as from UVB-rich light. Even modest exposure may directly reduce
Th1 cell activity, through some path other than that mediated by
vitamin D.
Just some thoughts, fwiw.
J.
| |
| randall 2006-04-20, 11:19 am |
|
JXStern wrote:
> On 19 Apr 2006 14:29:50 -0700, "bj" <bjmacc@msn.com> wrote:
>
> All good stuff, but if it were that simple, couldn't we just take a
> little extra vitamin D and be happy?
I took a lot of extra vitamin D that did little. SuPPose i needed
the nb-uvb to light it's fire? lol
Lets pumed it,
http://www.ncbi.nlm.nih.gov/entrez/...t_uids=16547967
1,25 dihydroxyvitamin-D3 modulates JAK-STAT pathway in IL-12/IFNgamma
axis leading to Th1 response in experimental allergic
encephalomyelitis.
Muthian G, Raikwar HP, Rajasingh J, Bright JJ.
Department of Neurology, Vanderbilt university Medical Center,
Nashville, Tennessee.
Experimental allergic encephalomyelitis (EAE) is a Th1 cell-mediated
autoimmune disease model of multiple sclerosis (MS). Vitamin D
deficiency is commonly observed in MS patients and vitamin D
supplements reduce the clinical symptoms of EAE and MS. Earlier studies
have shown that in vivo treatment with vitamin D analogs ameliorates
EAE in association with the inhibition of IL-12 production and Th1
differentiation. The mechanisms in the regulation of Th1 response by
vitamin D in EAE/MS are, however, not known. We show that in vivo
treatment of C57BL/6 and SJL/J mice (i.p.) with 100 ng of 1,25
dihydroxyvitamin D3, on every other day from Day 0-30, ameliorates EAE
in association with the inhibition of IL-12 production and neural
antigen-specific Th1 response. In vitro treatment with 1,25(OH)2D3
inhibited IFNgamma-induced tyrosine phosphorylation of STAT1, without
affecting JAK2, in EOC-20 microglial cells. Treatment of activated T
cells with 1,25(OH)2D3 also inhibited the IL-12-induced tyrosine
phosphorylation of JAK2, TYK2, STAT3, and STAT4 in association with a
decrease in T cell proliferation in vitro. These findings highlight the
fact that vitamin D modulates JAK-STAT signaling pathway in
IL-12/IFNgamma axis leading to Th1 differentiation and further suggest
its use in the treatment of MS and other Th1 cell-mediated autoimmune
diseases. (c) 2006 Wiley-Liss, Inc.
PMID: 16547967
or
http://www.ncbi.nlm.nih.gov/entrez/...t_uids=16543659
+
http://www.ncbi.nlm.nih.gov/entrez/...t_uids=16441425
[...]
Taken together, VitD3 strongly suppressed T-cell responses by
inhibiting functional differentiation of precursor dendritic cells into
functional BMDC1 that are feasible for inducing Th1-dependent cellular
immunity.
PMID: 16441425
Whoops, letter dude just came on. I wonder if Jay has better guests?
See ya!
randall... taking his vitD3 outa this equation for now.
>
> Therapeutic UVB is usually intense for much shorter than 20 minutes, I
> have no idea if that produces tons of vitamin D, or if more time at
> less intensity would be better. The doctors seem to like to get you
> on the edge of a burn, it doesn't seem to be a fixed-dose situation.
> Again, if it were, they could just tell you to get some sun - at least
> here in California, in the summer.
>
> I've gotten as much benefit from UVA tanning salon or winter/morning
> sun, as from UVB-rich light. Even modest exposure may directly reduce
> Th1 cell activity, through some path other than that mediated by
> vitamin D.
Read the link. Jak-stat!
>
> Just some thoughts, fwiw.
>
> J.
| |
|
| hi jx, i don't think it's simple..lol...it was just a cusory
explanation. Just vitamin D or just sun fail to work for me. I have
found it takes a couple of months to get a up the level of D and it
takes about a month to wait for the misfiring tcells to die off.
I quit banging the drum of my treatment., i experiment and report what
i find. uvb from lights while intense, and undoubtedly making vitamin D
still runs into the problem of dendritic and tcells with receptors
carryiing around bits of protein which it thinks are invaders. it takes
about a week for mature dendritic cells to die off and about a month
for the tcells to die off.
just a simple explanation
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