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STAT ER Time --- HIV and Psor GENETIC's --Wilson Liao-- > Juergen Schauber -> Cathelicidins (LL37) -- Vitamin D3 -AmPs --
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randall
May 15, 2012, 3:57:00 PM5/15/12
to
hi
I'm NOT dead YET:
see
Sat, May 12 2012 2:02 pm
Subject: I'm DEAD deaD DEADski! Are you, yet? Cardio &
Psoriasis...Heart ATTACK Events -->> Widow Maker -- Vitamin K2 &
Parkinson's --C/EBP -alpha Skin Cancer -- St John's WORT Cream- 5HTP
day -
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/780d0453d19752ac
and
Tues, May 15 2012 12:44 pm
Subject: PSOR CZAR CowBOY -- Psoriatical HIV Genetics ---->Wilson LiaO
-->CpG HyPomethylation Or G(EE) becomes A! { segue Dopamine &
Tyrosine} -- SEROTONIN JUNKIE -- JC Mathers - Folic Acid
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/41d24c75ca6b55fe
What keeps me from BEING DEAD?
Epigenetics? (B and C and D3 vitamins et al)
No, no ....randall TAR BABY, Smells like....
It's now mother nature and how you work and live in harmony!
OK... kewl..
STAT to the ER you psor MONKEY!
That's right...
the ERAP1 gene.... is so... so... you know!
rap, rap, rap.... rap, rap, rap, doing the erap...
doing the ERAP....
Sorta catchy huh?
But youse got to have the RIgHT psor GENE's bub to do this flake skin
ERAP...
so there...
If your a homocystinuria patient, YOU respond to simple vitamin B6
supplementation.
What is it for PSOR heads?
Folic acid?
Why?
We're on the CpG island of the BLUE porpoise?
And the purpose of a GENE is clear cut till you get flaky skin.
So stat...ER time:
http://www.ncbi.nlm.nih.gov/pubmed/22575366
Autoimmun Rev. 2012 May 7.
The putative role of endoplasmic reticulum aminopeptidases in
autoimmunity: Insights from genomic-wide association studies.
Fierabracci A, Milillo A, Locatelli F, Fruci D.
Source
Immunology Area, Bambino Gesù Children's Hospital IRCCS Rome.
Abstract
Autoimmune diseases represent a heterogeneous group of conditions
whose incidence is increasing worldwide. This has stimulated studies
on their etiopathogenesis, derived from a complex interaction between
genetic and environmental factors, aimed at finally improving
prevention and treatment of these diseases. In the autoimmune process,
immune responses are generated against self antigens presented by
Major Histocompatibility Complex (MHC) class I on the cell surface.
These peptide/MHC class I complexes are generated and assembled in the
endoplasmic reticulum (ER) through MHC class I antigen processing and
presentation machinery. In the ER, aminopeptidases ERAP1 and ERAP2
display distinct trimming activity before antigenic peptides are
loaded onto MHC class I molecules. The advent of new tools such as
genome-wide association studies (GWAS) has provided evidence for new
susceptibility loci and candidate genes playing a role in the
autoimmune process for the recognized immune function of their
transcripts. Genetic linkage has been discovered with MHC antigens and
various autoimmune conditions. Several recent GWAS showed the
importance of ERAP1 and ERAP2 in several autoimmune diseases,
including ankylosing spondylitis, insulin-dependent diabetes mellitus,
psoriasis, multiple sclerosis, Crohn's disease. In this review, we
first provide a general overview of ERAP1 and ERAP2 genes, their
biological functions and their relevancy in autoimmunity. We then
discuss the importance of GWAS and the case-control studies that
confirm the relevancy of ERAP single-nucleotide polymorphism (SNP)
associations and their linkage with particular MHC class I haplotypes,
supporting a putative functional role in the autoimmune process.
PMID: 22575366
=====================
Hey LOOK at ME! I'm better then an hiv persons' immunity!
Ha! Is this deja VU?
Toss those GAY Guys a marriage license... mister obama BUSH III...
http://www.ncbi.nlm.nih.gov/pubmed/22577363
PLoS Genet. 2012 Feb;8(2):e1002514. Epub 2012 Feb 16.
Psoriasis Patients Are Enriched for Genetic Variants That Protect
against HIV-1 Disease.
Chen H, Hayashi G, Lai OY, Dilthey A, Kuebler PJ, Wong TV, Martin MP,
Fernandez Vina MA, McVean G, Wabl M, Leslie KS, Maurer T, Martin JN,
Deeks SG, Carrington M, Bowcock AM, Nixon DF, Liao W.
Source
Department of Dermatology, University of California San Francisco, San
Francisco, California, United States of America.
Abstract
An important paradigm in evolutionary genetics is that of a delicate
balance between genetic variants that favorably boost host control of
infection but which may unfavorably increase susceptibility to
autoimmune disease. Here, we investigated whether patients with
psoriasis, a common immune-mediated disease of the skin, are enriched
for genetic variants that limit the ability of HIV-1 virus to
replicate after infection. We analyzed the HLA class I and class II
alleles of 1,727 Caucasian psoriasis cases and 3,581 controls and
found that psoriasis patients are significantly more likely than
controls to have gene variants that are protective against HIV-1
disease. This includes several HLA class I alleles associated with
HIV-1 control; amino acid residues at HLA-B positions 67, 70, and 97
that mediate HIV-1 peptide binding; and the deletion polymorphism
rs67384697 associated with high surface expression of HLA-C. We also
found that the compound genotype KIR3DS1 plus HLA-B Bw4-80I, which
respectively encode a natural killer cell activating receptor and its
putative ligand, significantly increased psoriasis susceptibility.
This compound genotype has also been associated with delay of
progression to AIDS. Together, our results suggest that genetic
variants that contribute to anti-viral immunity may predispose to the
development of psoriasis.
PMID: 22577363
OMG that was dejavu.... will omama bush III save their FREEDOM's?
OK move on DOT soros DORKs... LOL
And JUST one of the reasons my genetic's are better is LL37.
http://www.ncbi.nlm.nih.gov/pubmed/22577261
Ann Dermatol. 2012 May;24(2):126-35. Epub 2012 Apr 26.
Cathelicidin LL-37: an antimicrobial peptide with a role in
inflammatory skin disease.
Reinholz M, Ruzicka T, Schauber J.
Source
Department of Dermatology and Allergy, Ludwig-Maximilian-University,
Munich, Germany.
Abstract
Chronic inflammatory skin diseases such as atopic dermatitis,
psoriasis or rosacea are very common. Although their exact
pathogenesis is not completely understood all three diseases are
characterized by dysregulation of cutaneous innate immunity.
Cathelicidin LL-37 is an important effector molecule of innate
immunity in the skin and atopic dermatitis, psoriasis or rosacea show
defects in cathelicidin expression, function or processing. In atopic
dermatitis, cathelicidin induction might be disturbed resulting in
defective antimicrobial barrier function. In contrast, psoriasis is
characterized by overexpression of cathelicidin. However to date it is
unclear whether pro- or anti-inflammatory functions of cathelicidin
predominate in lesional skin in psoriasis. In rosacea, cathelicidin
processing is disturbed resulting in peptide fragments causing
inflammation, erythema and telangiectasias. In this review, the
current evidence on the role of cathelicidin LL-37 in the pathogenesis
of inflammatory skin diseases will be outlined. As cathelicidin LL-37
might also serve as a future treatment target potential novel
treatment strategies for those diseases will be discussed.
PMID: 22577261
56 hits for-Schauber J[Author]
http://www.ncbi.nlm.nih.gov/pubmed?term=Schauber%20J%5BAuthor%5D
wow... J Schauber has 16 of his 56 hits for psoriasis:
http://www.ncbi.nlm.nih.gov/pubmed?term=Schauber%20J%5BAuthor%5D%20psoria*
Thank YOU Juergen for HARD Work and helping psoriatic's across the
world.
#2 of 56 and 16:
In regards to Scauber's next one...
Duh i said this about sunshine and LL37 from day 1.. IOWs the sunshine
vitamin D also
has an immune lowering function while oral vitamin D3 doesn't..
Sunshine is THUS better way to build a D3 store in your body....if
your psoriatic or autoimmune?
Till winter blues hit, and you need it... want it... got's to HAVE
it..
Fly south snow bird...or
then go to town on D3 supplementations...
http://www.ncbi.nlm.nih.gov/pubmed/22509827
Exp Dermatol. 2012 May;21(5):327-30. doi: 10.1111/j.
1600-0625.2012.01459.x.
Cathelicidin LL-37: a defense molecule with a potential role in
psoriasis pathogenesis.
Dombrowski Y, Schauber J.
Source
Department of Dermatology and Allergy, Ludwig-Maximilian University,
Munich, Germany.
Abstract
Epidermal keratinocytes produce and secrete antimicrobial peptides
(AMPs) that subsequently form a chemical shield on the skin surface.
Cathelicidins are one family of AMPs in skin with various further
immune functions. Consequently, dysfunction of these peptides has been
implicated in the pathogenesis of inflammatory skin disease. In
particular, the cathelicidin LL-37 is overexpressed in inflamed skin
in psoriasis, binds to extracellular self-DNA released from dying
cells and converts self-DNA in a potent stimulus for plasmacytoid
dendritic cells (pDCs). Subsequently, pDCs secrete type I interferons
and trigger an auto-inflammatory cascade. Paradoxically, therapies
targeting the vitamin D pathway such as vitamin D analogues or UVB
phototherapy ameliorate cutaneous inflammation in psoriasis but
strongly induce cathelicidin expression in skin at the same time.
Current evidence now suggests that self-DNA present in the cytosol of
keratinocytes is also pro-inflammatory active and triggers IL-1β
secretion in psoriatic lesions through the AIM2 inflammasome. This
time, however, binding of LL-37 to self-DNA neutralizes DNA-mediated
inflammation. Hence, cathelicidin LL-37 shows contrasting roles in
skin inflammation in psoriasis and might serve as a target for novel
therapies for this chronic skin disease.
PMID: 22509827
next for shauber
Gosh now we KNOW it's Th17.... so why don't they acknowledge it's
coming FROM SFB? Huh?
SFB being:
http://en.wikipedia.org/wiki/Segmented_filamentous_bacteria
and
http://www.ncbi.nlm.nih.gov/pubmed/19836068
Induction of intestinal Th17 cells by segmented filamentous bacteria.
Ivanov II, Atarashi K, Manel N, Brodie EL, Shima T, Karaoz U, Wei D,
Goldfarb KC, Santee CA, Lynch SV, Tanoue T, Imaoka A, Itoh K, Takeda
K, Umesaki Y, Honda K, Littman DR.
[...] pmid: 19836068
So more then D3 is on the table in LOW UVB winter months.
If you're eating sauerkraut or kimchi full of L. Plantarum that EATS
the sFB your OK more or less... LOL
http://www.ncbi.nlm.nih.gov/pubmed/22402441
J Invest Dermatol. 2012 Mar 8. doi: 10.1038/jid.2011.486.
Vitamin D Analog Calcipotriol Suppresses the Th17 Cytokine-Induced
Proinflammatory S100 "Alarmins" Psoriasin (S100A7) and Koebnerisin
(S100A15) in Psoriasis.
Hegyi Z, Zwicker S, Bureik D, Peric M, Koglin S, Batycka-Baran A,
Prinz JC, Ruzicka T, Schauber J, Wolf R.
Source
Department of Dermatology and Allergology, Ludwig-Maximilian
University, Munich, Germany.
Abstract
The antimicrobial peptides (AMP) psoriasin (S100A7) and koebnerisin
(S100A15) are differently induced in psoriatic skin. They act
synergistically as chemoattractants and "alarmins" to amplify
inflammation in psoriasis. Th17 cytokines are key players in psoriasis
pathogenesis and vitamin D analogs feature anti-psoriatic effects;
both of these activities could be mediated through epidermal AMP
regulation. We show that supernatants of cultured psoriatic T cells
induce and release psoriasin and koebnerisin from keratinocytes and
the Th17 cytokines IL-17A, tumor necrosis factor-α, and IL-22
differently regulate psoriasin and koebnerisin reflecting their
distinct expression pattern in normal and psoriatic skin. IL-17A is
the principal inducer of both S100 and their expression is further
amplified by cooperating Th17 cytokines in the micromilieu of
psoriatic skin. Increased extracellular psoriasin and koebnerisin also
synergize as "alarmins" to prime epidermal keratinocytes for
production of immunotropic cytokines that further amplify the
inflammatory response. Treatment of psoriatic plaques with the vitamin
D analog calcipotriol interferes with the S100-mediated positive
feedback loop by suppressing the increased production of psoriasin and
koebnerisin in psoriatic skin and their Th17-mediated regulation in
epidermal keratinocytes. Thus, targeting the S100-amplification loop
could be a beneficial anti-inflammatory approach in psoriasis and
other inflammatory skin diseases.Journal of Investigative Dermatology
advance online publication, 8 March 2012; doi:10.1038/jid.2011.486.
PMID: 22402441
I'd love to READ this one....hint hint... LOL (please send it to
me...)
I think i'm going to send this to you? <w> Good idea!
http://www.ncbi.nlm.nih.gov/pubmed/21869610
Pathogenic DNA: cytosolic DNA promotes inflammation in psoriasis.
Schauber J, Dombrowski Y, Besch R.
Cell Cycle. 2011 Sep 15;10(18):3038-9. Epub 2011 Sep 15. No abstract
available.
PMID: 21869610
Is there a clue to the above here?:
I've posted his next one: PMID: 21562230 three times:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=PMID%3A+21562230+&start=0&scoring=d&
http://www.ncbi.nlm.nih.gov/pubmed/21562230
Cytosolic DNA triggers inflammasome activation in keratinocytes in
psoriatic lesions.
Dombrowski Y, Peric M, Koglin S, Kammerbauer C, Göss C, Anz D,
Simanski M, Gläser R, Harder J, Hornung V, Gallo RL, Ruzicka T, Besch
R, Schauber J.
Sci Transl Med. 2011 May 11;3(82):82ra38.
PMID: 21562230
full text:
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21562230/?tool=pubmed
This next Schuaber bears out sorta what i said above in regards D3/
LL37
and i must have got it by reading Dick Gallo abstracts... LOL
And we have FULL text on it... yipppppeeee
http://www.ncbi.nlm.nih.gov/pubmed/21519404
Dermatoendocrinol. 2011 Jan;3(1):18-22.
Impact of vitamin D3 on cutaneous immunity and antimicrobial peptide
expression.
Antal AS, Dombrowski Y, Koglin S, Ruzicka T, Schauber J.
Source
Department of Dermatology and Allergy; Ludwig-Maximilian-University;
Munich, Germany.
Abstract
Antimicrobial peptides (AMPs) are effectors of cutaneous innate
immunity and protect primarily against microbial infections. An array
of AMPs can be found in and on the skin. Those include peptides that
were first discovered for their antimicrobial properties but also
proteins with antimicrobial activity first characterized for their
activity as chemokines, enzymes, enzyme inhibitors and neuropeptides.
Cathelicidins were among the first families of AMPs discovered in
skin. They are now known to exert a dual role in innate immune
defense: they have direct antimicrobial activity and will also
initiate a host cellular response resulting in cytokine release,
inflammation and angiogenesis. Altered cathelicidin expression and
function was observed in several common inflammatory skin diseases
such as atopic dermatitis, rosacea and psoriasis. Until recently the
molecular mechanisms underlying cathelicidin regulation were not
known. Lately, vitamin D3 was identified as the major regulator of
cathelicidin expression and entered the spotlight as an immune
modulator with impact on both, innate and adaptive immunity. Therapies
targeting vitamin D3 signalling may provide novel approaches for the
treatment of infectious and inflammatory skin diseases by affecting
both innate and adaptive immune functions through AMP regulation.
PMID: 21519404
Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21519404/?tool=pubmed
If you want to ONLY look at the one figure in this full text:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3051848/figure/F1/
Figure 1
Model for UVB triggered vitamin D3 activation and cathelicidin
response in the skin. Photochemical conversion of 7-dehydrocholesterol
to calciol in the skin requires UVB irradiation. In keratinocytes two
subsequent hydroxylation steps mediated by CYP27A1 and CYP27B1 result
in active calcitriol/1a,25-dihydroxyvitamin D3 (1,25VitD3) that binds
to and activates the vitamin D receptor (VDR) in an autocrine manner.
Steroid receptor coactivator 3 (SRC3) complexes with the VDR and
recruits histone acetyltransferases which open up chromatin and
facilitate access to the cathelicidin gene. VDR binds to the vitamin D
response element (VDRE) in the cathelicidin promoter region and
activates transcription. Cathelicidin is synthesized as an inactive
pro-peptide (hCAP18) which is cleaved upon release to active LL-37 by
serine proteases.
<snip>
^^^^^^^^^^^^^^^^
Speaking of Dick..
Schauber does have a study with UCSD Gallo
#19 of 56:
http://www.ncbi.nlm.nih.gov/pubmed/19949065
J Immunol. 2010 Jan 1;184(1):369-78. Epub 2009 Nov 30.
The host defense peptide cathelicidin is required for NK cell-mediated
suppression of tumor growth.
Büchau AS, Morizane S, Trowbridge J, Schauber J, Kotol P, Bui JD,
Gallo RL.
Source
Division of Dermatology, Department of Medicine, University of
California San Diego, La Jolla, CA 92093, USA.
Abstract
Tumor surveillance requires the interaction of multiple molecules and
cells that participate in innate and the adaptive immunity.
Cathelicidin was initially identified as an antimicrobial peptide,
although it is now clear that it fulfills a variety of immune
functions beyond microbial killing. Recent data have suggested
contrasting roles for cathelicidin in tumor development. Because its
role in tumor surveillance is not well understood, we investigated the
requirement of cathelicidin in controlling transplantable tumors in
mice. Cathelicidin was observed to be abundant in tumor-infiltrating
NK1.1(+) cells in mice. The importance of this finding was
demonstrated by the fact that cathelicidin knockout mice (Camp(-/-))
permitted faster tumor growth than wild type controls in two different
xenograft tumor mouse models (B16.F10 and RMA-S). Functional in vitro
analyses found that NK cells derived from Camp(-/-) versus wild type
mice showed impaired cytotoxic activity toward tumor targets. These
findings could not be solely attributed to an observed perforin
deficiency in freshly isolated Camp(-/-) NK cells, because this
deficiency could be partially restored by IL-2 treatment, whereas
cytotoxic activity was still defective in IL-2-activated Camp(-/-) NK
cells. Thus, we demonstrate a previously unrecognized role of
cathelicidin in NK cell antitumor function.
PMID: 19949065
Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19949065/?tool=pubmed
Wow.. we are lucky to have people zeroing in on this thing called
FLAKE SKIN.
randall... thanks to Dedicated Scientists... Like Schauber and
Liao...
and Bowcock and Jordan (psors2 -card14 )
I'm NOT dead YET:
see
Sat, May 12 2012 2:02 pm
Subject: I'm DEAD deaD DEADski! Are you, yet? Cardio &
Psoriasis...Heart ATTACK Events -->> Widow Maker -- Vitamin K2 &
Parkinson's --C/EBP -alpha Skin Cancer -- St John's WORT Cream- 5HTP
day -
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/780d0453d19752ac
and
Tues, May 15 2012 12:44 pm
Subject: PSOR CZAR CowBOY -- Psoriatical HIV Genetics ---->Wilson LiaO
-->CpG HyPomethylation Or G(EE) becomes A! { segue Dopamine &
Tyrosine} -- SEROTONIN JUNKIE -- JC Mathers - Folic Acid
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/41d24c75ca6b55fe
What keeps me from BEING DEAD?
Epigenetics? (B and C and D3 vitamins et al)
No, no ....randall TAR BABY, Smells like....
It's now mother nature and how you work and live in harmony!
OK... kewl..
STAT to the ER you psor MONKEY!
That's right...
the ERAP1 gene.... is so... so... you know!
rap, rap, rap.... rap, rap, rap, doing the erap...
doing the ERAP....
Sorta catchy huh?
But youse got to have the RIgHT psor GENE's bub to do this flake skin
ERAP...
so there...
If your a homocystinuria patient, YOU respond to simple vitamin B6
supplementation.
What is it for PSOR heads?
Folic acid?
Why?
We're on the CpG island of the BLUE porpoise?
And the purpose of a GENE is clear cut till you get flaky skin.
So stat...ER time:
http://www.ncbi.nlm.nih.gov/pubmed/22575366
Autoimmun Rev. 2012 May 7.
The putative role of endoplasmic reticulum aminopeptidases in
autoimmunity: Insights from genomic-wide association studies.
Fierabracci A, Milillo A, Locatelli F, Fruci D.
Source
Immunology Area, Bambino Gesù Children's Hospital IRCCS Rome.
Abstract
Autoimmune diseases represent a heterogeneous group of conditions
whose incidence is increasing worldwide. This has stimulated studies
on their etiopathogenesis, derived from a complex interaction between
genetic and environmental factors, aimed at finally improving
prevention and treatment of these diseases. In the autoimmune process,
immune responses are generated against self antigens presented by
Major Histocompatibility Complex (MHC) class I on the cell surface.
These peptide/MHC class I complexes are generated and assembled in the
endoplasmic reticulum (ER) through MHC class I antigen processing and
presentation machinery. In the ER, aminopeptidases ERAP1 and ERAP2
display distinct trimming activity before antigenic peptides are
loaded onto MHC class I molecules. The advent of new tools such as
genome-wide association studies (GWAS) has provided evidence for new
susceptibility loci and candidate genes playing a role in the
autoimmune process for the recognized immune function of their
transcripts. Genetic linkage has been discovered with MHC antigens and
various autoimmune conditions. Several recent GWAS showed the
importance of ERAP1 and ERAP2 in several autoimmune diseases,
including ankylosing spondylitis, insulin-dependent diabetes mellitus,
psoriasis, multiple sclerosis, Crohn's disease. In this review, we
first provide a general overview of ERAP1 and ERAP2 genes, their
biological functions and their relevancy in autoimmunity. We then
discuss the importance of GWAS and the case-control studies that
confirm the relevancy of ERAP single-nucleotide polymorphism (SNP)
associations and their linkage with particular MHC class I haplotypes,
supporting a putative functional role in the autoimmune process.
PMID: 22575366
=====================
Hey LOOK at ME! I'm better then an hiv persons' immunity!
Ha! Is this deja VU?
Toss those GAY Guys a marriage license... mister obama BUSH III...
http://www.ncbi.nlm.nih.gov/pubmed/22577363
PLoS Genet. 2012 Feb;8(2):e1002514. Epub 2012 Feb 16.
Psoriasis Patients Are Enriched for Genetic Variants That Protect
against HIV-1 Disease.
Chen H, Hayashi G, Lai OY, Dilthey A, Kuebler PJ, Wong TV, Martin MP,
Fernandez Vina MA, McVean G, Wabl M, Leslie KS, Maurer T, Martin JN,
Deeks SG, Carrington M, Bowcock AM, Nixon DF, Liao W.
Source
Department of Dermatology, University of California San Francisco, San
Francisco, California, United States of America.
Abstract
An important paradigm in evolutionary genetics is that of a delicate
balance between genetic variants that favorably boost host control of
infection but which may unfavorably increase susceptibility to
autoimmune disease. Here, we investigated whether patients with
psoriasis, a common immune-mediated disease of the skin, are enriched
for genetic variants that limit the ability of HIV-1 virus to
replicate after infection. We analyzed the HLA class I and class II
alleles of 1,727 Caucasian psoriasis cases and 3,581 controls and
found that psoriasis patients are significantly more likely than
controls to have gene variants that are protective against HIV-1
disease. This includes several HLA class I alleles associated with
HIV-1 control; amino acid residues at HLA-B positions 67, 70, and 97
that mediate HIV-1 peptide binding; and the deletion polymorphism
rs67384697 associated with high surface expression of HLA-C. We also
found that the compound genotype KIR3DS1 plus HLA-B Bw4-80I, which
respectively encode a natural killer cell activating receptor and its
putative ligand, significantly increased psoriasis susceptibility.
This compound genotype has also been associated with delay of
progression to AIDS. Together, our results suggest that genetic
variants that contribute to anti-viral immunity may predispose to the
development of psoriasis.
PMID: 22577363
OMG that was dejavu.... will omama bush III save their FREEDOM's?
OK move on DOT soros DORKs... LOL
And JUST one of the reasons my genetic's are better is LL37.
http://www.ncbi.nlm.nih.gov/pubmed/22577261
Ann Dermatol. 2012 May;24(2):126-35. Epub 2012 Apr 26.
Cathelicidin LL-37: an antimicrobial peptide with a role in
inflammatory skin disease.
Reinholz M, Ruzicka T, Schauber J.
Source
Department of Dermatology and Allergy, Ludwig-Maximilian-University,
Munich, Germany.
Abstract
Chronic inflammatory skin diseases such as atopic dermatitis,
psoriasis or rosacea are very common. Although their exact
pathogenesis is not completely understood all three diseases are
characterized by dysregulation of cutaneous innate immunity.
Cathelicidin LL-37 is an important effector molecule of innate
immunity in the skin and atopic dermatitis, psoriasis or rosacea show
defects in cathelicidin expression, function or processing. In atopic
dermatitis, cathelicidin induction might be disturbed resulting in
defective antimicrobial barrier function. In contrast, psoriasis is
characterized by overexpression of cathelicidin. However to date it is
unclear whether pro- or anti-inflammatory functions of cathelicidin
predominate in lesional skin in psoriasis. In rosacea, cathelicidin
processing is disturbed resulting in peptide fragments causing
inflammation, erythema and telangiectasias. In this review, the
current evidence on the role of cathelicidin LL-37 in the pathogenesis
of inflammatory skin diseases will be outlined. As cathelicidin LL-37
might also serve as a future treatment target potential novel
treatment strategies for those diseases will be discussed.
PMID: 22577261
56 hits for-Schauber J[Author]
http://www.ncbi.nlm.nih.gov/pubmed?term=Schauber%20J%5BAuthor%5D
wow... J Schauber has 16 of his 56 hits for psoriasis:
http://www.ncbi.nlm.nih.gov/pubmed?term=Schauber%20J%5BAuthor%5D%20psoria*
Thank YOU Juergen for HARD Work and helping psoriatic's across the
world.
#2 of 56 and 16:
In regards to Scauber's next one...
Duh i said this about sunshine and LL37 from day 1.. IOWs the sunshine
vitamin D also
has an immune lowering function while oral vitamin D3 doesn't..
Sunshine is THUS better way to build a D3 store in your body....if
your psoriatic or autoimmune?
Till winter blues hit, and you need it... want it... got's to HAVE
it..
Fly south snow bird...or
then go to town on D3 supplementations...
http://www.ncbi.nlm.nih.gov/pubmed/22509827
Exp Dermatol. 2012 May;21(5):327-30. doi: 10.1111/j.
1600-0625.2012.01459.x.
Cathelicidin LL-37: a defense molecule with a potential role in
psoriasis pathogenesis.
Dombrowski Y, Schauber J.
Source
Department of Dermatology and Allergy, Ludwig-Maximilian University,
Munich, Germany.
Abstract
Epidermal keratinocytes produce and secrete antimicrobial peptides
(AMPs) that subsequently form a chemical shield on the skin surface.
Cathelicidins are one family of AMPs in skin with various further
immune functions. Consequently, dysfunction of these peptides has been
implicated in the pathogenesis of inflammatory skin disease. In
particular, the cathelicidin LL-37 is overexpressed in inflamed skin
in psoriasis, binds to extracellular self-DNA released from dying
cells and converts self-DNA in a potent stimulus for plasmacytoid
dendritic cells (pDCs). Subsequently, pDCs secrete type I interferons
and trigger an auto-inflammatory cascade. Paradoxically, therapies
targeting the vitamin D pathway such as vitamin D analogues or UVB
phototherapy ameliorate cutaneous inflammation in psoriasis but
strongly induce cathelicidin expression in skin at the same time.
Current evidence now suggests that self-DNA present in the cytosol of
keratinocytes is also pro-inflammatory active and triggers IL-1β
secretion in psoriatic lesions through the AIM2 inflammasome. This
time, however, binding of LL-37 to self-DNA neutralizes DNA-mediated
inflammation. Hence, cathelicidin LL-37 shows contrasting roles in
skin inflammation in psoriasis and might serve as a target for novel
therapies for this chronic skin disease.
PMID: 22509827
next for shauber
Gosh now we KNOW it's Th17.... so why don't they acknowledge it's
coming FROM SFB? Huh?
SFB being:
http://en.wikipedia.org/wiki/Segmented_filamentous_bacteria
and
http://www.ncbi.nlm.nih.gov/pubmed/19836068
Induction of intestinal Th17 cells by segmented filamentous bacteria.
Ivanov II, Atarashi K, Manel N, Brodie EL, Shima T, Karaoz U, Wei D,
Goldfarb KC, Santee CA, Lynch SV, Tanoue T, Imaoka A, Itoh K, Takeda
K, Umesaki Y, Honda K, Littman DR.
[...] pmid: 19836068
So more then D3 is on the table in LOW UVB winter months.
If you're eating sauerkraut or kimchi full of L. Plantarum that EATS
the sFB your OK more or less... LOL
http://www.ncbi.nlm.nih.gov/pubmed/22402441
J Invest Dermatol. 2012 Mar 8. doi: 10.1038/jid.2011.486.
Vitamin D Analog Calcipotriol Suppresses the Th17 Cytokine-Induced
Proinflammatory S100 "Alarmins" Psoriasin (S100A7) and Koebnerisin
(S100A15) in Psoriasis.
Hegyi Z, Zwicker S, Bureik D, Peric M, Koglin S, Batycka-Baran A,
Prinz JC, Ruzicka T, Schauber J, Wolf R.
Source
Department of Dermatology and Allergology, Ludwig-Maximilian
University, Munich, Germany.
Abstract
The antimicrobial peptides (AMP) psoriasin (S100A7) and koebnerisin
(S100A15) are differently induced in psoriatic skin. They act
synergistically as chemoattractants and "alarmins" to amplify
inflammation in psoriasis. Th17 cytokines are key players in psoriasis
pathogenesis and vitamin D analogs feature anti-psoriatic effects;
both of these activities could be mediated through epidermal AMP
regulation. We show that supernatants of cultured psoriatic T cells
induce and release psoriasin and koebnerisin from keratinocytes and
the Th17 cytokines IL-17A, tumor necrosis factor-α, and IL-22
differently regulate psoriasin and koebnerisin reflecting their
distinct expression pattern in normal and psoriatic skin. IL-17A is
the principal inducer of both S100 and their expression is further
amplified by cooperating Th17 cytokines in the micromilieu of
psoriatic skin. Increased extracellular psoriasin and koebnerisin also
synergize as "alarmins" to prime epidermal keratinocytes for
production of immunotropic cytokines that further amplify the
inflammatory response. Treatment of psoriatic plaques with the vitamin
D analog calcipotriol interferes with the S100-mediated positive
feedback loop by suppressing the increased production of psoriasin and
koebnerisin in psoriatic skin and their Th17-mediated regulation in
epidermal keratinocytes. Thus, targeting the S100-amplification loop
could be a beneficial anti-inflammatory approach in psoriasis and
other inflammatory skin diseases.Journal of Investigative Dermatology
advance online publication, 8 March 2012; doi:10.1038/jid.2011.486.
PMID: 22402441
I'd love to READ this one....hint hint... LOL (please send it to
me...)
I think i'm going to send this to you? <w> Good idea!
http://www.ncbi.nlm.nih.gov/pubmed/21869610
Pathogenic DNA: cytosolic DNA promotes inflammation in psoriasis.
Schauber J, Dombrowski Y, Besch R.
Cell Cycle. 2011 Sep 15;10(18):3038-9. Epub 2011 Sep 15. No abstract
available.
PMID: 21869610
Is there a clue to the above here?:
I've posted his next one: PMID: 21562230 three times:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=PMID%3A+21562230+&start=0&scoring=d&
http://www.ncbi.nlm.nih.gov/pubmed/21562230
Cytosolic DNA triggers inflammasome activation in keratinocytes in
psoriatic lesions.
Dombrowski Y, Peric M, Koglin S, Kammerbauer C, Göss C, Anz D,
Simanski M, Gläser R, Harder J, Hornung V, Gallo RL, Ruzicka T, Besch
R, Schauber J.
Sci Transl Med. 2011 May 11;3(82):82ra38.
PMID: 21562230
full text:
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21562230/?tool=pubmed
This next Schuaber bears out sorta what i said above in regards D3/
LL37
and i must have got it by reading Dick Gallo abstracts... LOL
And we have FULL text on it... yipppppeeee
http://www.ncbi.nlm.nih.gov/pubmed/21519404
Dermatoendocrinol. 2011 Jan;3(1):18-22.
Impact of vitamin D3 on cutaneous immunity and antimicrobial peptide
expression.
Antal AS, Dombrowski Y, Koglin S, Ruzicka T, Schauber J.
Source
Department of Dermatology and Allergy; Ludwig-Maximilian-University;
Munich, Germany.
Abstract
Antimicrobial peptides (AMPs) are effectors of cutaneous innate
immunity and protect primarily against microbial infections. An array
of AMPs can be found in and on the skin. Those include peptides that
were first discovered for their antimicrobial properties but also
proteins with antimicrobial activity first characterized for their
activity as chemokines, enzymes, enzyme inhibitors and neuropeptides.
Cathelicidins were among the first families of AMPs discovered in
skin. They are now known to exert a dual role in innate immune
defense: they have direct antimicrobial activity and will also
initiate a host cellular response resulting in cytokine release,
inflammation and angiogenesis. Altered cathelicidin expression and
function was observed in several common inflammatory skin diseases
such as atopic dermatitis, rosacea and psoriasis. Until recently the
molecular mechanisms underlying cathelicidin regulation were not
known. Lately, vitamin D3 was identified as the major regulator of
cathelicidin expression and entered the spotlight as an immune
modulator with impact on both, innate and adaptive immunity. Therapies
targeting vitamin D3 signalling may provide novel approaches for the
treatment of infectious and inflammatory skin diseases by affecting
both innate and adaptive immune functions through AMP regulation.
PMID: 21519404
Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21519404/?tool=pubmed
If you want to ONLY look at the one figure in this full text:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3051848/figure/F1/
Figure 1
Model for UVB triggered vitamin D3 activation and cathelicidin
response in the skin. Photochemical conversion of 7-dehydrocholesterol
to calciol in the skin requires UVB irradiation. In keratinocytes two
subsequent hydroxylation steps mediated by CYP27A1 and CYP27B1 result
in active calcitriol/1a,25-dihydroxyvitamin D3 (1,25VitD3) that binds
to and activates the vitamin D receptor (VDR) in an autocrine manner.
Steroid receptor coactivator 3 (SRC3) complexes with the VDR and
recruits histone acetyltransferases which open up chromatin and
facilitate access to the cathelicidin gene. VDR binds to the vitamin D
response element (VDRE) in the cathelicidin promoter region and
activates transcription. Cathelicidin is synthesized as an inactive
pro-peptide (hCAP18) which is cleaved upon release to active LL-37 by
serine proteases.
<snip>
^^^^^^^^^^^^^^^^
Speaking of Dick..
Schauber does have a study with UCSD Gallo
#19 of 56:
http://www.ncbi.nlm.nih.gov/pubmed/19949065
J Immunol. 2010 Jan 1;184(1):369-78. Epub 2009 Nov 30.
The host defense peptide cathelicidin is required for NK cell-mediated
suppression of tumor growth.
Büchau AS, Morizane S, Trowbridge J, Schauber J, Kotol P, Bui JD,
Gallo RL.
Source
Division of Dermatology, Department of Medicine, University of
California San Diego, La Jolla, CA 92093, USA.
Abstract
Tumor surveillance requires the interaction of multiple molecules and
cells that participate in innate and the adaptive immunity.
Cathelicidin was initially identified as an antimicrobial peptide,
although it is now clear that it fulfills a variety of immune
functions beyond microbial killing. Recent data have suggested
contrasting roles for cathelicidin in tumor development. Because its
role in tumor surveillance is not well understood, we investigated the
requirement of cathelicidin in controlling transplantable tumors in
mice. Cathelicidin was observed to be abundant in tumor-infiltrating
NK1.1(+) cells in mice. The importance of this finding was
demonstrated by the fact that cathelicidin knockout mice (Camp(-/-))
permitted faster tumor growth than wild type controls in two different
xenograft tumor mouse models (B16.F10 and RMA-S). Functional in vitro
analyses found that NK cells derived from Camp(-/-) versus wild type
mice showed impaired cytotoxic activity toward tumor targets. These
findings could not be solely attributed to an observed perforin
deficiency in freshly isolated Camp(-/-) NK cells, because this
deficiency could be partially restored by IL-2 treatment, whereas
cytotoxic activity was still defective in IL-2-activated Camp(-/-) NK
cells. Thus, we demonstrate a previously unrecognized role of
cathelicidin in NK cell antitumor function.
PMID: 19949065
Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19949065/?tool=pubmed
Wow.. we are lucky to have people zeroing in on this thing called
FLAKE SKIN.
randall... thanks to Dedicated Scientists... Like Schauber and
Liao...
and Bowcock and Jordan (psors2 -card14 )
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