HLA-Cw6 (psors1) -- Chinese HAN & PSORs4 SNP - HAX-1 - IL22 & Psor/IBD -- αvβ8 integrin & SFB vs Th17 -- Resveratrol increased--->Sirtuin1 block STAT3? --
randall
<warning:: far reaching effects of these genes (below) affect psor and
IBD/colitis folk)
--------------------------------------
HLA-Cw6 - AKA - PSORS1
9 hits - hla-cw6 - OMIM
http://www.ncbi.nlm.nih.gov/sites/entrez?db=omim&cmd=DetailsSearch&term=hla-cw6
LOOK at this in the first one:
HLA-Cw6 protects against viremia and hiv/aids:
http://www.ncbi.nlm.nih.gov/omim/142840#AllelicVariants-142840
A little flake here and there isn't so bad compared to Th2 and no
TNF in the GAME to wipe out those pesky little virals.
Sheessh... i hate it when folks die due to some virus. :(
STOP the underhanded virals...and skin plaque and IBD pain
in the you know what...
OK how?
Finding homeostasis...?
1st................the players (genes) in the game.
HLA-C
http://www.ncbi.nlm.nih.gov/gene/3107
[...] Also known as HLC-C; D6S204; HLA-Cw; PSORS1; HLA-JY3; FLJ27082;
HLA-C
Summary HLA-C belongs to the HLA class I heavy chain paralogues. This
class I molecule is a heterodimer consisting of a heavy chain and a
light chain (beta-2 microglobulin). The heavy chain is anchored in the
membrane. Class I molecules play a central role in the immune system
by presenting peptides derived from endoplasmic reticulum lumen. They
are expressed in nearly all cells. The heavy chain is approximately 45
kDa and its gene contains 8 exons. Exon one encodes the leader
peptide, exons 2 and 3 encode the alpha1 and alpha2 domain, which both
bind the peptide, exon 4 encodes the alpha3 domain, exon 5 encodes the
transmembrane region, and exons 6 and 7 encode the cytoplasmic tail.
Polymorphisms within exon 2 and exon 3 are responsible for the peptide
binding specificity of each class one molecule. Typing for these
polymorphisms is routinely done for bone marrow and kidney
transplantation. Over one hundred HLA-C alleles have been described
<sniP>
you moron--> this stuff helps to kill those virals. LOL
LCE3C_LCE3B (late cornified envelope 3c & 3) Ties psors1 to psors4
and lce3c and lce3b:
4 hits - entrez gene - for LCE3C LCE3B
http://www.ncbi.nlm.nih.gov/sites/entrez?db=gene&cmd=DetailsSearch&term=LCE3C_LCE3B
So we have ____Bowcock, Elder____ and ALL these other wonderful psor
scientists nailing our psor SKIN.
http://www.ncbi.nlm.nih.gov/pubmed/21107349
J Invest Dermatol. 2010 Nov 25.
Meta-Analysis Confirms the LCE3C_LCE3B Deletion as a Risk Factor for
Psoriasis in Several Ethnic Groups and Finds Interaction with HLA-Cw6.
Riveira-Munoz E, He SM, Escaramís G, Stuart PE, Hüffmeier U, Lee C,
Kirby B, Oka A, Giardina E, Liao W, Bergboer J, Kainu K, de Cid R,
Munkhbat B, Zeeuwen PL, Armour JA, Poon A, Mabuchi T, Ozawa A,
Zawirska A, Burden AD, Barker JN, Capon F, Traupe H, Sun LD, Cui Y,
Yin XY, Chen G, Lim HW, Nair RP, Voorhees JJ, Tejasvi T, Pujol R,
Munkhtuvshin N, Fischer J, Kere J, Schalkwijk J, Bowcock A, Kwok PY,
Novelli G, Inoko H, Ryan AW, Trembath RC, Reis A, Zhang XJ, Elder JT,
Estivill X.
Genes and Disease Programme, Center for Genomic Regulation (CRG) and
Public Health and Epidemiology Network Biomedical Research Center
(CIBERESP), Barcelona, Spain.
Abstract
A multicenter meta-analysis including data from 9,389 psoriasis
patients and 9,477 control subjects was performed to investigate the
contribution of the deletion of genes LCE3C and LCE3B, involved in
skin barrier defense, to psoriasis susceptibility in different
populations. The study confirms that the deletion of LCE3C and LCE3B
is a common genetic factor for susceptibility to psoriasis in the
European populations (OR(Overall)=1.21 (1.15-1.27)), and for the first
time directly demonstrates the deletion's association with psoriasis
in the Chinese (OR=1.27 (1.16-1.34)) and Mongolian (OR=2.08
(1.44-2.99)) populations. The analysis of the HLA-Cw6 locus showed
significant differences in the epistatic interaction with the LCE3C
and LCE3B deletion in at least some European populations, indicating
epistatic effects between these two major genetic contributors to
psoriasis. The study highlights the value of examining genetic risk
factors in multiple populations to identify genetic interactions, and
indicates the need of further studies to understand the interaction of
the skin barrier and the immune system in susceptibility to
psoriasis.Journal of Investigative Dermatology advance online
publication, 25 November 2010; doi:10.1038/jid.2010.350.
PMID: 21107349
A BIG kudos to Estivill X:
8 hits - "Estivill X"[Author] AND psoria* - pubmed:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=%22Estivill+X%22%5BAuthor%5D+AND+psoria*
Don't you love it when these scientists from around the world
actually figure out whats haPPening?
Sure do...NO surPrise there. :)
=====================================
Psors4 is at Iq21
http://www.ncbi.nlm.nih.gov/pubmed/11348461
Fine mapping of the PSORS4 psoriasis susceptibility region on
chromosome 1q21.
[...] PMID: 11348461
Full text
http://dx.doi.org/10.1046/j.1523-1747.2001.01311.x
7 hits - 1q21 psors4 - pubmed:
http://www.ncbi.nlm.nih.gov/pubmed?term=1q21%20psors4&itool=QuerySuggestion
13 hits - psors4 - pubmed (GENE)
http://www.ncbi.nlm.nih.gov/gene?term=%20psors4
http://en.wikipedia.org/wiki/Han_Chinese
[...] Han Chinese constitute about 92% of the population of the
People's Republic of China (mainland China), 98% of the population of
the Republic of China (Taiwan), 78% of the population of Singapore,
and about 20% of the entire global human population.
<sniP>
http://www.ncbi.nlm.nih.gov/pubmed/21109726
Dermatology. 2010 Nov 27.
The Association between the IL-20 -1723C→G Allele on the 1q Chromosome
and Psoriasis Triggered or Exacerbated by an Upper Respiratory Tract
Infection in the Chinese Han Population.
Chen XY, Jin LW, Chen YW, Tian H, Yuan WT, Niu ZM, Zhang J, Huang W,
Zheng J.
Department of Dermatology, Ruijin Hospital, School of Medicine,
Shanghai Jiaotong University, Shanghai, China.
Abstract
Background: Psoriasis is a cutaneous disorder of multifactorial
etiology influenced by both genetic and environmental factors such as
infection. Methods: We conducted a genome analysis with 20
microsatellite markers spanning the long arm of chromosome 1 in 36
Chinese families with psoriasis and detected evidence for linkage at
1q21 with a nonparametric linkage score of 1.74, p = 0.03, and 1q32
with one of 1.84, p = 0.03. According to the positional and functional
candidate principle, we further investigated the single-nucleotide
polymorphisms of the HAX-1 gene (located in 1q21) and IL-20 gene
(located in 1q32) in a case-control study including 340 sporadic
patients and 199 controls. Results: We determined that the frequency
of the G allele of IL-20 -1723C→G (rs1713239) was significantly higher
among psoriatic patients (38.5% in cases vs. 31.2% in controls, p =
0.015, odds ratio, OR = 1.39, 95% confidence interval, CI =
1.07-1.80). When we stratified our analysis by psoriasis triggered or
exacerbated by infection of the upper respiratory tract, a significant
difference was detected (42.4% in stratified cases vs. 31.2% in
controls, p = 0.005, OR = 1.63, 95% CI = 1.15-2.30). Conclusion: We
assume that triggered or exacerbated by respiratory tract infection,
the population with the G allele of IL-20 -1723C→G are predisposed to
psoriasis.
Copyright © 2010 S. Karger AG, Basel.
PMID: 21109726
if this was a kofi post it would be over. <w>
Whew...
SS my word... well... i've never. <g> ;~/
And it would have been TWO seParate posts of two abstracts.
And no halofuginone in the GAME. LOL
Heck no nothing in those naked abstractions. <G>
Hey i'm GLAD kofi posted a hydrangea halofuginone abstract. LOL
3 hits : 1q32 AND IL-20 [ pubmed - entrez gene]
http://www.ncbi.nlm.nih.gov/sites/entrez?db=gene&cmd=DetailsSearch&term=1q32+IL-20
Two of those 3 hits: {IL20, IL19 but not IL24}
IL-20 entrez gene:
http://www.ncbi.nlm.nih.gov/gene/50604
[...] Also known as IL-20; IL10D; ZCYTO10; MGC96907; IL20
Summary The protein encoded by this gene is a cytokine structurally
related to interleukin 10 (IL10). This cytokine has been shown to
transduce its signal through signal transducer and activator of
transcription 3 (STAT3) in keratinocytes. A specific receptor for this
cytokine is found to be expressed in skin and upregulated dramatically
in psoriatic skin, suggesting a role for this protein in epidermal
function and psoriasis.
<snip>
http://www.ncbi.nlm.nih.gov/gene/29949
[...] Also known as MDA1; NG.1; ZMDA1; IL-10C; IL19
Summary The protein encoded by this gene is a cytokine that belongs to
the IL10 cytokine subfamily. This cytokine is found to be
preferentially expressed in monocytes. It can bind the IL20 receptor
complex and lead to the activation of the signal transducer and
activator of transcription 3 (STAT3). A similar cytokine in mouse is
reported to up-regulate the expression of IL6 and TNF-alpha and induce
apoptosis, which suggests a role of this cytokine in inflammatory
responses. Alternatively spliced transcript variants encoding the
distinct isoforms have been described.
<snip>
----
9 hits - IL20 AND psoriasis
http://www.ncbi.nlm.nih.gov/sites/entrez?db=gene&cmd=DetailsSearch&term=IL-20+psoriasis
1723C - an snP strep thing protein in the SR or ER?
http://www.ncbi.nlm.nih.gov/gene?term=1723C
For all databases pretty sparse:
http://www.ncbi.nlm.nih.gov/sites/gquery?term=1723C
OK found it. SNP
http://www.ncbi.nlm.nih.gov/projects/SNP/snp_ref.cgi?rs=4931030
[...] HGVS Names
NG_008626.1:g.145150C>T
NM_139241.2:c.*1723C>T
NT_009714.17:g.25555314C>T
HGVs
http://phencode.bx.psu.edu/faq.html#dots
Why didn't i know that?
Why would YOU? LOL
IL-20 G Allele -
http://www.ncbi.nlm.nih.gov/gene?term=IL-20%20G%20allele
61 hits - hax-1
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=hax-1
HAX-1 HAX1 HCLS1 associated protein X-1
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=retrieve&dopt=full_report&list_uids=10456
[...] Also known as SCN3; HS1BP1; HCLSBP1; FLJ17042; FLJ18492;
FLJ93803; HAX1
Summary The protein encoded by this gene is known to associate with
hematopoietic cell-specific Lyn substrate 1, a substrate of Src family
tyrosine kinases. It also interacts with the product of the polycystic
kidney disease 2 gene, mutations in which are associated with
autosomal-dominant polycystic kidney disease, and with the F-actin-
binding protein, cortactin. It was earlier thought that this gene
product is mainly localized in the mitochondria, however, recent
studies indicate it to be localized in the cell body. Mutations in
this gene result in autosomal recessive severe congenital neutropenia,
also known as Kostmann disease. Two transcript variants encoding
different isoforms have been found for this gene.
<snip>
http://www.ncbi.nlm.nih.gov/pubmed/19913549
J Mol Cell Cardiol. 2010 Jun;48(6):1266-79. Epub 2009 Nov 11.
HAX-1: a multifaceted antiapoptotic protein localizing in the
mitochondria and the sarcoplasmic reticulum of striated muscle cells.
Yap SV, Vafiadaki E, Strong J, Kontrogianni-Konstantopoulos A.
University of Maryland, School of Medicine, Department of Biochemistry
and Molecular Biology, Baltimore, MD 21201, USA.
Abstract
HAX-1 comprises a family of ubiquitously expressed proteins with
antiapoptotic properties. In the current study, we investigated
HAX-1's temporospatial distribution in rat striated muscles during
development and in adulthood. In cardiocytes, HAX-1 is organized at
the level of Z-disks throughout embryogenesis and adulthood; however,
in skeletal myofibers, it is in register with M-bands during embryonic
and early postnatal life and Z-disks during late postnatal and adult
life. Immunoelectron microscopy and subcellular fractionation
demonstrated that HAX-1 proteins localize at the mitochondrial and
sarcoplasmic reticulum (SR) membranes, as well as at sites where the
two are closely apposed. Variants I and II selectively concentrate in
the mitochondrial membranes, whereas variants III, IV, and V localize
in both organelles, albeit to varying extents. Deletion analysis
combined with cellular transfections indicated that elimination of
HAX-1's NH(2)-terminus abolishes its mitochondrial targeting and
attenuates its antiapoptotic capacity, while removal of its binding
site for the SR protein phospholamban (PLN) prevents its translocation
to the SR. Consistent with this, HAX-1 is preferentially lost from the
SR of PLN-deficient hearts. Our findings are the first to present a
comprehensive characterization of HAX-1's expression in striated
muscles and to provide insights on the mechanisms through which it may
modulate apoptosis.
(PMID: 19913549
http://en.wikipedia.org/wiki/Endoplasmic_reticulum#Sarcoplasmic_reticulum
http://www.ncbi.nlm.nih.gov/pubmed/19524642
Biochim Biophys Acta. 2009 Oct;1790(10):1139-48. Epub 2009 Jun 12.
HAX-1: a multifunctional protein with emerging roles in human disease.
Fadeel B, Grzybowska E.
Division of Molecular Toxicology, Institute of Environmental Medicine,
Karolinska Institutet, 171 77 Stockholm, Sweden. bengt....@ki.se
Abstract
HS-1-associated protein X-1 (HAX-1) was identified more than 10 years
ago as a novel protein with ubiquitous tissue expression and a
predominantly mitochondrial localization at the subcellular level.
Recent studies have shown that homozygous mutations in the HAX1 gene
are associated with autosomal recessive forms of severe congenital
neutropenia (also known as Kostmann disease), and results from studies
in mice and men are beginning to unravel a prominent role for HAX-1 in
apoptosis signaling not only in the hematopoietic compartment, but
also in the central nervous system. Moreover, several different
cellular and viral binding partners of HAX-1 have been identified thus
pointing toward a complex and multifunctional role of this protein.
HAX-1 has also been shown to bind to the 3' untranslated regions of
certain mRNAs and could therefore contribute to the regulation of
transport and/or stability of such transcripts. The present review
discusses the emerging and divergent roles of HAX-1, including its
involvement in cell migration, apoptosis signaling, and mRNA
surveillance. The importance of HAX-1 in human disease is also
highlighted and outstanding questions that remain to be addressed are
identified.
PMID: 19524642
http://www.ncbi.nlm.nih.gov/pubmed/19920172
Proc Natl Acad Sci U S A. 2009 Dec 8;106(49):20776-81. Epub 2009 Nov
17.
The anti-apoptotic protein HAX-1 is a regulator of cardiac function.
Zhao W, Waggoner JR, Zhang ZG, Lam CK, Han P, Qian J, Schroder PM,
Mitton B, Kontrogianni-Konstantopoulos A, Robia SL, Kranias EG.
Department of Pharmacology and Cell Biophysics, University of
Cincinnati College of Medicine, Cincinnati, OH 45267-0575, USA.
Abstract
The HS-1 associated protein X-1 (HAX-1) is a ubiquitously expressed
protein that protects cardiomyocytes from programmed cell death. Here
we identify HAX-1 as a regulator of contractility and calcium cycling
in the heart. HAX-1 overexpression reduced sarcoplasmic reticulum Ca-
ATPase (SERCA2) pump activity in isolated cardiomyocytes and in vivo,
leading to depressed myocyte calcium kinetics and mechanics.
Conversely, downregulation of HAX-1 enhanced calcium cycling and
contractility. The inhibitory effects of HAX-1 were abolished upon
phosphorylation of phospholamban, which plays a fundamental role in
controlling basal contractility and constitutes a key downstream
effector of the beta-adrenergic signaling cascade. Mechanistically,
HAX-1 promoted formation of phospholamban monomers, the active/
inhibitory units of the calcium pump. Indeed, ablation of PLN rescued
HAX-1 inhibition of contractility in vivo. Thus, HAX-1 represents a
regulatory mechanism in cardiac calcium cycling and its responses to
sympathetic stimulation, implicating its importance in calcium
homeostasis and cell survival.
PMID: 19920172
===============================================
And since we've (psoriatics) have got this viral protection via
psors1 et al.....calling all IL-22 to the forefront line of immunity.
Can't we just have half the trooPs on the front line? LOL
http://www.ncbi.nlm.nih.gov/pubmed/21106435
Cytokine Growth Factor Rev. 2010 Nov 22.
Distinct roles of IL-22 in human psoriasis and inflammatory bowel
disease.
Ouyang W.
Department of Immunology, Genentech, Inc., 1 DNA Way, M/S 34, South
San Francisco, CA 94080, USA.
Abstract
IL-22, an IL-10 family cytokine, is produced by different leukocyte
subsets, including T cells, NK cells and lymphoid tissue inducer (LTi)
cells. IL-22 mediates the crosstalk between leukocytes and tissue
epithelia because its receptor is preferentially expressed on various
tissue epithelial cells. IL-22 is essential for host defense against
infections of extracellular pathogens, such as bacteria and yeasts, by
eliciting various innate defensive mechanisms from tissue epithelial
cells and promoting wound-healing responses. In autoimmune diseases,
however, diverse tissue microenvironments and underlying pathogenic
mechanisms may result in opposing contributions of IL-22 in disease
progression. For example, in psoriasis, IL-22 can synergize with other
proinflammatory cytokines to induce many of the pathogenic phenotypes
from keratinocytes and exacerbate disease progression. In contrast,
IL-22 plays a beneficial role in IBD by enhancing barrier integrity
and epithelial innate immunity of intestinal tract.
PMID: 21106435
OK, so gut flora will knock this pest back IMO.
-------------------------
SO WHATs :LACKing in OUR colons?
http://en.wikipedia.org/wiki/TGF_beta_Activation
[...] Loss of αvβ8 integrin on dendritic cells causes autoimmunity and
colitis.
how abutt αvβ8 integrin then?
Yeah?
OK i mean dis and dat:
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=omim&Cmd=ShowDetailView&TermToSearch=604160
MIM ID *604160MGI, -- INTEGRIN, BETA-8; ITGB8
But first we do that αvβ8 integrin and psor.
And i think we have to MUCH of this αvβ8 integrin. :(
http://www.ncbi.nlm.nih.gov/pubmed/21099117
J Clin Invest. 2010 Nov 22. pii: 43786. doi: 10.1172/JCI43786.
Expression of αvβ8 integrin on dendritic cells regulates Th17 cell
development and experimental autoimmune encephalomyelitis in mice.
Melton AC, Bailey-Bucktrout SL, Travis MA, Fife BT, Bluestone JA,
Sheppard D.
Abstract
Th17 cells promote a variety of autoimmune diseases, including
psoriasis, multiple sclerosis, rheumatoid arthritis, and inflammatory
bowel disease. TGF-β is required for conversion of naive T cells to
Th17 cells, but the mechanisms regulating this process are unknown.
Integrin αvβ8 on DCs can activate TGF-β, and this process contributes
to the development of induced Tregs. Here, we have now shown that
integrin αvβ8 expression on DCs plays a critical role in the
differentiation of Th17 cells. Th17 cells were nearly absent in the
colons of mice lacking αvβ8 expression on DCs. In addition, these mice
and the DCs harvested from them had an impaired ability to convert
naive T cells into Th17 cells in vivo and in vitro, respectively.
Importantly, mice lacking αvβ8 on DCs showed near-complete protection
from experimental autoimmune encephalomyelitis. Our results therefore
suggest that the integrin αvβ8 pathway is biologically important and
that αvβ8 expression on DCs could be a therapeutic target for the
treatment of Th17-driven autoimmune disease.
PMID: 21099117
But wouldn't lower amounts of SFB (segmented filamentous bacterium)
also
lower the Th17?
Ans: YES/
SFB must be more then an enigma in these pathways.
Certainly blocking (similar to blocking TNF with biologicals) SFB
would
eliminate the need to block the integrin?
------------------------------
WOW sitT1 and psor?
http://www.ncbi.nlm.nih.gov/pubmed/21098725
FASEB J. 2010 Nov 23. [Epub ahead of print]
STAT3-dependent effects of IL-22 in human keratinocytes are
counterregulated by sirtuin 1 through a direct inhibition of STAT3
acetylation.
Sestito R, Madonna S, Scarponi C, Cianfarani F, Failla CM, Cavani A,
Girolomoni G, Albanesi C.
*Laboratory of Experimental Immunology and.
Abstract
IL-22 has a pathogenetic role in psoriasis, where it is responsible
for the altered proliferation and differentiation of keratinocytes and
induces inflammatory molecules. The IL-22-induced effects are mediated
by STAT3, whose activity is proportional to acetylation in lysine
(Lys)685 and phosphorylation in tyrosine (Tyr)705. Lys 685 acetylation
of STAT3 is inhibited by sirtuin (SIRT)1, a class III deacetylase
promoting keratinocyte differentiation. Due to the opposite effects of
IL-22 and SIRT1, we investigated whether IL-22-induced effects in
keratinocytes could be regulated by SIRT1 through control of STAT3. We
found that SIRT1 opposes the IL-22-induced STAT3 activity by
deacetylating STAT3 and reducing STAT3 Tyr705 phosphorylation. By
controlling STAT3, SIRT1 also influences the IL-22-induced expression
of molecules involved in proliferation and inflammation as well as
proliferation and migration processes in cultured keratinocytes.
Although SIRT1 levels were similar in keratinocytes of healthy
individuals and patients with psoriasis, they were reduced in
psoriatic skin lesions, with the lymphokine IFN-γ inhibiting SIRT1
expression. Concomitantly, IFN-γ enhanced basal acetylation of STAT3
and its phosphorylation induced by IL-22. In conclusion, STAT3-
dependent IL-22 signaling and effects in keratinocytes are negatively
regulated by SIRT1. In skin affected by psoriasis, SIRT1 is down-
regulated by IFN-γ, which thus renders psoriatic keratinocytes more
prone to respond to IL-22.-Sestito, R., Madonna, S., Scarponi, C.,
Cianfarani, F., Failla, C. M., Cavani, A., Girolomoni, G., Albanesi,
C. STAT3-dependent effects of IL-22 in human keratinocytes are
counterregulated by sirtuin 1 through a direct inhibition of STAT3
acetylation.
PMID: 21098725
OK so as psoriatic with all those virus fighting TNF's and IFN's we
just take some suPPlemental resveratrol and block STAT3 by
uPregulating SirT1 via resveratrol?
Sounds like a dead drunk proposition to psor heads who drink red
mountain
by the gallon. <w>
Take longevinex supplements instead. LOL
----------------------------------------
http://www.ncbi.nlm.nih.gov/pubmed/21098395
Blood. 2010 Nov 22.
Human neutrophils interact with both 6-sulfo LacNAc+ DC and NK cells
to amplify NK-derived IFN{gamma}: role of CD18, ICAM-1 and ICAM-3.
Costantini C, Calzetti F, Perbellini O, Micheletti A, Scarponi C,
Lonardi S, Pelletier M, Schakel K, Pizzolo G, Facchetti F, Vermi W,
Albanesi C, Cassatella MA.
Department of Pathology and Diagnostics, Division of General
Pathology, University of Verona, Verona, Italy;
Abstract
The role of neutrophils as key players in the regulation of innate and
adaptive immune responses is increasingly being recognized. Here, we
report that human neutrophils establish a network with both NK cells
and 6-sulfo LacNAc(+) dendritic cells (slanDC), which ultimately
serves to upregulate NK-derived IFNγ. This network involves direct
reciprocal interactions as well as positive amplification loops
mediated by cell-derived cytokines. Accordingly, we show that after
LPS plus IL-2- or IL-15/IL-18-stimulation, neutrophils directly
interact with and potentiate the activity of both slanDC and NK cells.
On the one hand, neutrophils augment the release of IL-12p70 by slanDC
via a CD18/ICAM-1 interaction that, in turn, stimulates activated NK
cells to produce IFNγ. IFNγ, in turn, further potentiates the
interaction between neutrophils and slanDC and the release of slanDC-
derived IL-12p70, thus creating a positive feedback loop. On the other
hand, neutrophils directly co-stimulate NK cells via CD18/ICAM-3,
leading to the production of IFNγ. Co-localization of neutrophils, NK
cells and slanDC, as well as of IL-12p70 and IFNγ, in inflamed tissues
of Crohn's disease and psoriasis provides strong evidence for a novel
cellular and cytokine cooperation within the innate immune system in
which neutrophils act as amplifiers of NK cell/slanDC-mediated
responses.
PMID: 21098395
OK so block LPS with good gut flora...
And IFN will go down to a respectable level and so will your psor
plaques.
===========================================
Tnf blocker inducts psoriasis de novo?
You know oh?
http://www.ncbi.nlm.nih.gov/pubmed/21099241
Korean J Gastroenterol. 2010 Nov 25;56(5):324-328.
[A Case of Psoriasis Induced by Infliximab Treatment for Crohn's
Disease.]
[Article in Korean]
Jwa YJ, Kim NH, Park HJ, Park JS, Bae WK, Kim KA, Lee JS, Moon YS.
Departments of Internal Medicine, lsan Paik Hospital, Inje University
College of Medicine, Goyang, Korea.
Abstract
Infliximab, the monoclonal antibody to tumor necrosis factor, is
indicated for refractory luminal and fistulizing Crohn's disease and
rheumatoid arthritis. Infliximab treatment has adverse events
including infusion reactions, opportunistic infections, and the
potential for the event such as reactivation of latent tuberculosis.
Cutaneous adverse reactions of TNF-α agents include skin rash,
urticaria, pruritus, lupus-like eruption, and injection site
reactions. Most of all, psoriasis or psoriasiform dermatitis induced
by infliximab treatment for Crohn's disease is rarely reported in
Korea. We report a case of psoriasis induced by infliximab treatment
for Crohn's disease with a review of world literature.
PMID: 21099241
--------------------------
randall... wow... kewl post/ thread and nails crohn's and psoriasis
genes...
Kofi
<52d2f087-8300-4e55...@n2g2000pre.googlegroups.com>,
randall <ranh...@aol.com> wrote:
SIRT1 inducers:
fasting [PMID 20148352]
PPARalpha agonists [PMID 17164430]
melatonin [PMID 19650880]
ketogenic diet
branched-chain amino acids (leucine, isoleucine, valine)
exercise [PMID 19913571]
Avoid glucosamine
<http://www.sciencedaily.com/releases/2010/10/101027111349.htm>
Check my posts in sci.life-extension on PPARalpha, SIRT1, etc.
> Tnf blocker inducts psoriasis de novo?
If psoriasis is caused by an underlying infection, it would make sense.
Inhibiting TNF-alpha would leave one more vulnerable to infection.