LACTOBACILLUS PLANTARUM for PSOR heads INST$EAD of TNF Blockers?
randall
And then the mother rat said, who will help me make the cake?
And no psor RAT said a thing.
And then mother rizzo said who will BE CLEAR with sweet whey and
l. plantarum imPlants?
Oh criPes...
I'm not even getting this.
I will soon enough, but till then it's kimchi.
I'd do better with a ratso rizzo line or two?
http://www.imdb.com/title/tt0064665/quotes
[...]
Ratso Rizzo: I'm walking here! I'm walking here!
<sniP>
I'll simply amend it to say I'm eating kimchi here! <W>
Did I really say excrement in that last PSOR post?
Maybe I should have said extramint?
This is the WEB and some of us should try to remain polite. LOL
And did BILL really sing this to HILLARY once the DNA on
the BLUE DRESS was FOUND?
http://www.youtube.com/watch?v=0B2ebg8butg
she wore blue velvet-parapapapapaparara
If only the stuPid LAME media did the same for BILL as TIGER?
To late now.
It's a small wonder the muslims want to kill the american PIGs. LOL
If only they knew the art of LUAU.
But, but...
Little american pigs like soros and david Plouffe always
carPing and harPing on left weird leaning values. LOL
http://www.examiner.com/x-32781-Clarksburg-Conservative-Examiner~y2009m12d16-George-Soros-and-Obama-enemies-of-liberty
Did they mean the enema of freedom?
So the left has taken over amerika and BIG PIG Gov?
http://en.wikipedia.org/wiki/David_Plouffe
http://en.wikipedia.org/wiki/David_Axelrod
http://en.wikipedia.org/wiki/Rahm_Emanuel
NO WHEY... soros is taking a cue and blaming obama for
listening to him. LOL
Who is this big pig gov guy?
http://biggovernment.com/2009/12/15/soros-wants-imf-to-subsidize-his-green-investments/
SWEET...
I want the current pussy cat in soro's lap, in the oval office to know
this:
Dems are more FUN when their like Bill & monica:
http://www.youtube.com/watch?v=nOgCaDYbEsY
When they become serious like Psoriatic Stalin with psor skin in the
game...
Then their more like me. LOL
I made the sunspots stoP.
No really. You have to watch those PSOR heads. LOL
But their due back. I don't want an ice age NOW.
Well... i'd rather play with m...
Hey you ... get off my keyboard....
darn four legged critters....
What's new
http://www.youtube.com/watch?v=VBdSqk78nHw&NR=1&feature=fvwp
Mine are a lot cuter then this one.
http://www.youtube.com/watch?v=ImBW1N5321Q
I want a strong Pussy Cat Doll?
Yikes
http://www.youtube.com/watch?v=Uf2Zjw8b4qA&feature=related
Now i need some real music.
From Russia with LOVE?
http://www.youtube.com/watch?v=ygJYxMP_ICY
Now that is REAL music. LOL
I wonder what the gills are for?
Must be a veiled attemPt at russian sarcasm or a commentary on
cold water?
I like this pyrotechnic cynical russian Vitas....gilled guy.
I'll find more tube you for him.
Hey.... did he do the 5th element?
I think he did. The caption says:
**VITAS and DIVA of 5th Element**
Oh wait. It's a mix. I like the real one better.
http://en.wikipedia.org/wiki/The_Fifth_Element#Soundtrack
http://en.wikipedia.org/wiki/Inva_Mula-Tchako
http://en.wikipedia.org/wiki/Inva_Mula-Tchako#Brief_incursion_in_the_film_industry
What made me think of this?
I forgot..must be tau protein in the neuronal cells?
Yu say neuronal i say glia. What do those glia glue cells do?
http://www.psychologytoday.com/blog/the-new-brain/200912/glia-the-other-brain
Oh wait. I did see the Ten tenors last sunday. Did enjoy them.
They had a christmas Theme going with one of their regular shows.
===============
BrAIN muSt work...
WoRk brain cells....
Ok...
Oh wait... this is my L. P> trial thread.
Is L. Plantarum immunopotentiating for higher TREG levels?
And is there a there THERE for proteotoxicity in the ER in
this psor equation?
STAT
http://www.jci.org/articles/view/15020/version/1
Does any of this make sense? LOL
Of course not. It's all sPin like the BIG PIG gov boys do. <G>
AT any rate...
That is my latest trial.
Will L. Plantarum decrease the suspected SFB (segmented filamentous
bacterium ) and allow expansion of treg's?
Time will tell and so WILL i. :)
The players:
A short line up with more later perhaPs?
T cells
http://en.wikipedia.org/wiki/T_cell
http://en.wikipedia.org/wiki/T_cell#Regulatory
Regulatory T cells (Treg cells), formerly known as suppressor T cells,
are crucial for the maintenance of immunological tolerance. Their
major role is to shut down T cell-mediated immunity toward the end of
an immune reaction and to suppress auto-reactive T cells that escaped
the process of negative selection in the thymus. Two major classes of
CD4+ regulatory T cells have been described, including the naturally
occurring Treg cells and the adaptive Treg cells. Naturally occurring
Treg cells (also known as CD4+CD25+FoxP3+ Treg cells) arise in the
thymus, whereas the adaptive Treg cells (also known as Tr1 cells or
Th3 cells) may originate during a normal immune response. Naturally
occurring Treg cells can be distinguished from other T cells by the
presence of an intracellular molecule called FoxP3. Mutations of the
FOXP3 gene can prevent regulatory T cell development, causing the
fatal autoimmune disease IPEX.
<sniP>
All THINGs Regulatory (as in T cells)
http://en.wikipedia.org/wiki/Regulatory_T_cell
http://en.wikipedia.org/wiki/FOXP3
Symbols FOXP3; AIID; DIETER; IPEX; JM2; MGC141961; MGC141963; PIDX;
XPID
FOXP3 (forkhead box P3) is a gene involved in immune system responses.
A member of the FOX protein family, FOXP3 appears to function as the
master regulator in the development and function of regulatory T cells.
[1]
While the precise control mechanism has not yet been established, FOX
proteins belong to the forkhead/winged-helix family of transcriptional
regulators and are presumed to exert control via similar DNA binding
interactions during transcription.
[...]
Physiology
The discovery of Foxp3 as a specific marker of natural T regulatory
cells (nTregs, a lineage of T cells) and adaptive/induced T regulatory
(a/iTregs) T cells has recently led to an explosion of research in the
biological properties of regulatory T cells (Tregs).[4][5][6] In
animal studies, Tregs that express Foxp3 are critical in the transfer
of immune tolerance, especially self-tolerance, so that hopefully in
the future this knowledge can be used to prevent transplant graft
rejection. The induction or administration of Foxp3 positive T cells
has, in animal studies, led to marked reductions in (autoimmune)
disease severity in models of diabetes, multiple sclerosis, asthma,
inflammatory bowel disease, thyroiditis and renal disease.[7] These
discoveries give hope that cellular therapies using Foxp3 positive
cells may, one day, help overcome these diseases. Unfortunately recent
T cell biology investigations revealed that T cell nature is much more
plastic than initially thought. Thus the regulatory T cell therapy may
in fact be very risky as the T regulatory cell transferred to the
patient may reverse and become another proinflammatory T cell.(see
recent papers from Romagnani, Stockinger etc). Th17 (T helper 17)
cells are proinflammatory and are produced under very similar
environments as a/iTregs. Th17 cells are produced under the influence
of TGF-β and IL-6 (or IL-21) whereas a/iTregs are produced under the
influence of solely TGF-β and as such the difference between a
proinflammatory and a pro-regulatory scenario is the presence of a
single interleukin (IL-6 or IL-21 is being debated by immunology
laboratories as the definitive signaling molecule). It seems so far
that murine studies point to IL-6 whereas human studies have shown
IL-21 (a Harvard study).
Pathophysiology
In human disease, alterations in numbers of regulatory T cells – and
in particular those that express Foxp3 – are found in a number of
disease states. For example, patients with tumors have a local
relative excess of Foxp3 positive T cells which inhibits the body's
ability to suppress the formation of cancerous cells.[8] Conversely,
patients with an autoimmune disease such as systemic lupus
erythematosus (SLE) have a relative dysfunction of Foxp3 positive
cells.[9] The Foxp3 gene is also mutated in the X-linked IPEX syndrome
(Immunodysregulation, Polyendocrinopathy, and Enteropathy, X-linked).
[10] These mutations were in the forkhead domain of FOXP3, indicating
that the mutations may disrupt critical DNA interactions.
In mice, a Foxp3 mutation (a frameshift mutation that result in
protein lacking the forkhead domain) is responsible for 'Scurfy', an X-
linked recessive mouse mutant that results in lethality in hemizygous
males 16 to 25 days after birth.[11] These mice have overproliferation
of CD4+ T-lymphocytes, extensive multiorgan infiltration, and
elevation of numerous cytokines. This phenotype is similar to those
that lack expression of CTLA-4, TGF-β, human disease IPEX, or deletion
of the Foxp3 gene in mice ("scurfy mice"). The pathology observed in
scurfy mice seems to result from an inability to properly regulate
CD4+ T-cell activity. In mice overexpressing the Foxp3 gene, fewer T
cells are observed. The remaining T cells have poor proliferative and
cytolytic responses and poor interleukin-2 production, although thymic
development appears normal. Histologic analysis indicates that
peripheral lymphoid organs, particularly lymph nodes, lack the proper
number of cells.
<sniP>
To increase FoxP3 and Treg's and decrease Th17 and SFB;s...
That is the question...
And i'm a little clearer already. :)
With that cast of character's even Watson would think Sherlock was
pulling the wool over his furrowed brows...
Oh... must watch the robert downey jr. version this christmas:
http://www.movieweb.com/news/NE9wqiacDl6qbh
-----------------
But can't we trust a rat first?
Sure.... same genes without the psor ones.
I bet if we could increase their life spans it would show up?
Old psor rats live forever in a Parallel universe.
You are them. LOL
www.ncbi.nlm.nih.gov/pubmed/19998507
2009 Dec 14;15(46):5843-50.
Changes in intestinal mucosal immune barrier in rats with endotoxemia.
Liu C, Li A, Weng YB, Duan ML, Wang BE, Zhang SW.
Department of Infectious Disease and Critical Care Medicine, Beijing
Friendship Hospital Affiliated to Capital Medical University, No. 95
Yongan Road, Xuanwu District, Beijing 100050, China.
zsw4...@sina.com.
AIM: To investigate the dysfunction of the immunological barrier of
the intestinal mucosa during endotoxemia and to elucidate the
potential mechanism of this dysfunction. METHODS: Male Wistar rats
were randomly distributed into two groups: control group and
lipopolysaccharide (LPS) group. Endotoxemia was induced by a single
caudal venous injection of LPS. Animals were sacrificed in batches 2,
6, 12 and 24 h after LPS infusion. The number of microfold (M)-cells,
dendritic cells (DCs), CD4(+) T cells, CD8(+) T cells, regulatory T
(Tr) cells and IgA(+) B cells in the intestinal mucosa were counted
after immunohistochemical staining. Apoptotic lymphocytes were counted
after TUNEL staining. The levels of interleukin (IL)-4, interferon
(IFN)-gamma and forkhead box P3 (Foxp3) in mucosal homogenates were
measured by ELISA. The secretory IgA (sIgA) content in the total
protein of one milligram of small intestinal mucus was detected using
a radioimmunological assay. RESULTS: This research demonstrated that
LPS-induced endotoxemia results in small intestinal mucosa injury. The
number of M-cells, DCs, CD8(+) T cells, and IgA(+) B cells were
decreased while Tr cell and apoptotic lymphocyte numbers were
increased significantly. The number of CD4(+) T cells increased in the
early stages and then slightly decreased by 24 h. The level of IL-4
significantly increased in the early stages and then reversed by the
end of the study period. The level of IFN-gamma increased slightly in
the early stages and then decreased markedly by the 24 h time point.
Level of Foxp3 increased whereas sIgA level decreased. CONCLUSION:
Mucosal immune dysfunction forms part of the intestinal barrier injury
during endotoxemia. The increased number and function of Tr cells as
well as lymphocyte apoptosis result in mucosal immunodeficiency.
PMID: 19998507
www.ncbi.nlm.nih.gov/pubmed/19997968
J Clin Immunol. 2009 Dec 9. [Epub ahead of print]
Frequency of Treg Cells Is Reduced in CVID Patients with Autoimmunity
and Splenomegaly and Is Associated with Expanded CD21(lo) B
Lymphocytes.
Arumugakani G, Wood PM, Carter CR.
Department of Clinical Immunology, Beckett Wing, St.James's University
Hospital, Leeds, UK, LS9 7TF, gururaj_dr @yahoo.com.
INTRODUCTION: Common variable immunodeficiency is a heterogeneous
antibody deficiency syndrome with autoimmune and inflammatory
complications in a significant proportion of patients. The study was
designed to evaluate the role of T regulatory (Treg) cells in common
variable immunodeficiency (CVID) patients with autoimmunity. METHODS:
The number and frequency of Treg cells (CD4(+), CD25(hi), Foxp3(+))
were evaluated in patients and controls, and Foxp3 expression in
different subgroups of CVID patients with common clinical
manifestations was compared. RESULTS: CVID patients had significantly
fewer Treg cells than controls, and low frequency of Treg cells was
associated with expansion of CD21(lo) B cells in patients. Patients
with autoimmunity had significantly reduced frequency but normal
numbers of regulatory T cells, whilst patients with splenomegaly had
significant reduction in frequency and number of regulatory T cells.
CONCLUSION: Foxp3 is useful on its own or as an adjunct to classify
CVID patients although the possibility of reduction in Treg cells as a
secondary phenomenon cannot be excluded.
PMID: 19997968
==================
I know... i'll do some current things and see if they blend in.
Sounds stuPid...
I know i am what are yuou?
http://www.pharmatimes.com/WorldNews/article.aspx?id=17072
[...]
In the past week,Roche has terminated a cancer collaboration with
Genmab and pulled out of a pact with Actelion to develop the latter’s
selective sphingosine 1-phosphate receptor 1 (S1P1) agonist for
psoriasis and multiple sclerosis.
<sniP>
Why hit on the S1P1 pathway?
www.ncbi.nlm.nih.gov/pubmed/19483717
Nat Immunol. 2009 Jul;10(7):769-77. Epub 2009 May 31.
The receptor S1P1 overrides regulatory T cell-mediated immune
suppression through Akt-mTOR.
Liu G, Burns S, Huang G, Boyd K, Proia RL, Flavell RA, Chi H.
Department of Immunology, St. Jude Children's Research Hospital,
Memphis, Tennessee, USA.
Regulatory T cells (T(reg) cells) are critically involved in
maintaining immunological tolerance, but this potent suppression must
be 'quenched' to allow the generation of adaptive immune responses.
Here we report that sphingosine 1-phosphate (S1P) receptor type 1
(S1P1) delivers an intrinsic negative signal to restrain the thymic
generation, peripheral maintenance and suppressive activity of T(reg)
cells. Combining loss- and gain-of-function genetic approaches, we
found that S1P1 blocked the differentiation of thymic T(reg)
precursors and function of mature T(reg) cells and affected T(reg)
cell-mediated immune tolerance. S1P1 induced selective activation of
the Akt-mTOR kinase pathway to impede the development and function of T
(reg) cells. Dynamic regulation of S1P1 contributed to lymphocyte
priming and immune homeostasis. Thus, by antagonizing T(reg) cell-
mediated immune suppression, the lipid-activated S1P1-Akt-mTOR pathway
orchestrates adaptive immune responses.
PMID: 19483717
------------
Ten hits in our group for S1P1
http://groups.google.com/groups/search?hl=en&q=psoriasis+s1p1+randall&sitesearch=
============
Ok, more cast of characters for the Psor oPera... down under and
toPical. <W>
keyword: cd103 psoriasis [8 returns P NG]
http://groups.google.com/groups/search?hl=en&q=cd103+psoriasis&btnG=Search&sitesearch=
http://en.wikipedia.org/wiki/ITGAE
Integrin, alpha E (ITGAE) also known as CD103 (Cluster of
Differentiation 103) is an integrin.[1] CD103 binds integrin beta 7
(β7– ITGB7) to form the complete heterodimeric integrin molecule αEβ7,
which has no distinct name. The αEβ7 complex is often referred to as
"CD103" though this appellation strictly refers only to the αE chain.
Note that the β7 subunit can bind with other integrin α chains, such
as α4 (CD49d).
Tissue Distribution
CD103 is expressed widely on intraepithelial lymphocyte (IEL) T cells
(both αβ T cells and γδ T cells) and on some peripheral regulatory T
cells (Tregs).[2] It has also been reported on lamina propria T cells.
[3]
Function
The chief ligand for αEβ7 is E-cadherin, an adhesion molecule (CAM)
found on epithelial cells.[4] It is probably important for T cell
homing to the intestinal sites.[5]
Tregs are important for decreasing the immune response and appear to
play a crucial role in the prevention of autoimmune diseases. Tregs
are defined as CD4+/CD25+/Foxp3+ cells.[6] Some CD4+/FoxP3- cells also
express CD103 and have been attributed regulatory activity. It is
unclear whether the presence of CD103 on Treg cells represents a
specialized feature for Treg, or Treg differentiation of IEL T cells.
---------
http://en.wikipedia.org/wiki/ITGB7
http://en.wikipedia.org/wiki/EED
Polycomb protein EED is a protein that in humans is encoded by the EED
gene.
Function
Polycomb protein EED is a member of the Polycomb-group (PcG) family.
PcG family members form multimeric protein complexes, which are
involved in maintaining the transcriptional repressive state of genes
over successive cell generations. This protein interacts with enhancer
of zeste 2, the cytoplasmic tail of integrin β7, immunodeficiency
virus type 1 (HIV-1) MA protein, and histone deacetylase proteins.
This protein mediates repression of gene activity through histone
deacetylation, and may act as a specific regulator of integrin
function. Two transcript variants encoding distinct isoforms have been
identified for this gene.[3]
Interactions
EED has been shown to interact with HDAC1,[4] Histone deacetylase 2,
[4] PPP1R8,[5] TGS1,[6] EZH2[7][4][8] and ITGB7.[1]
==============
HDAC interactions?
This one comes from some Joe in Montana...
You don't say. <w>
www.ncbi.nlm.nih.gov/pubmed/19011628
Nat Immunol. 2009 Jan;10(1):92-100. Epub 2008 Nov 16.
The histone deacetylase HDAC11 regulates the expression of interleukin
10 and immune tolerance.
Villagra A, Cheng F, Wang HW, Suarez I, Glozak M, Maurin M, Nguyen D,
Wright KL, Atadja PW, Bhalla K, Pinilla-Ibarz J, Seto E, Sotomayor EM.
Division of Immunology, H. Lee Moffitt Cancer Center and Research
Institute, Tampa, Florida 33612, USA.
Erratum in:
Nat Immunol. 2009 Jun;10(6):665.
Comment in:
Nat Immunol. 2009 Jan;10(1):13-4.
Antigen-presenting cells (APCs) induce T cell activation as well as T
cell tolerance. The molecular basis of the regulation of this critical
'decision' is not well understood. Here we show that HDAC11, a member
of the HDAC histone deacetylase family with no prior defined
physiological function, negatively regulated expression of the gene
encoding interleukin 10 (IL-10) in APCs. Overexpression of HDAC11
inhibited IL-10 expression and induced inflammatory APCs that were
able to prime naive T cells and restore the responsiveness of tolerant
CD4+ T cells. Conversely, disruption of HDAC11 in APCs led to
upregulation of expression of the gene encoding IL-10 and impairment
of antigen-specific T cell responses. Thus, HDAC11 represents a
molecular target that influences immune activation versus immune
tolerance, a critical 'decision' with substantial implications in
autoimmunity, transplantation and cancer immunotherapy.
PMID: 19011628
This Sotomayor author is rocking it.
Didn't obama have a de soto decision also?
No... his was an edsel of a suPreme decision and now
he takes credit for Stimulust:
http://www.startribune.com/business/79248937.html?elr=KArks:DCiU1OiP:DiiUiD3aPc:_Yyc:aUU
I love how he blames BUSH and then takes credit for preventing the
collapse
of capitalism and then causes craPitalism to eventual horizon collaPse
anyway. LOL
Wow---> moron thoughts from a stuPidly psor man. <G>
Whoops___> segue to stuPidly is over and OUT.
-----------------------------------------------------
Let's see what's new or older for IL-10
A newer one:
www.ncbi.nlm.nih.gov/pubmed/19555720
Immunol Lett. 2009 Aug 15;125(2):114-8. Epub 2009 Jun 23.
TLR5 ligation by flagellin converts tolerogenic dendritic cells into
activating antigen-presenting cells that preferentially induce T-
helper 1 responses.
Vicente-Suarez I, Brayer J, Villagra A, Cheng F, Sotomayor EM.
Division of Immunology and Division of Malignant Hematology, H. Lee
Moffitt Cancer Center & Research Institute, Tampa, FL 33612, United
States.
Dendritic cells (DCs) differentiated in the presence of IL-10
preferentially induce regulatory T-cells and tolerance. Whether the
tolerogenic properties displayed by these DCs (Tol-DCs) can be
overcome has not been fully explored. Here we show for the first time
that Tol-DCs express higher levels of TLR5 mRNA, but not TLR4 or TLR9
mRNA relative to DCs differentiated with GM-CSF and IL-4 (BM-DCs). In
response to flagellin, a natural TLR-5 ligand, Tol-DCs produced IL-12
but not IL-10. Unlike Tol-DCs stimulated with LPS, which produce high
levels of IL-10 and fail to generate a cognate inflammatory response
in CD4(+) T-cells, flagellin-stimulated Tol-DCs promoted the
differentiation of CD4(+) T cells with a T-helper 1 phenotype. The
divergent T-cell outcomes induced by Tol-DCs in response to different
TLR-ligands highlights not only their plasticity, but also points to
TLR5 ligation as a potential strategy to overcome tolerance in
environments that are otherwise conducive to immune unresponsiveness.
PMID: 19555720
And an older sotomayor iL-10:
Eur J Immunol. 2007 Nov;37(11):3164-75.
Identification of a novel negative role of flagellin in regulating
IL-10 production.
Vicente-Suarez I, Takahashi Y, Cheng F, Horna P, Wang HW, Wang HG,
Sotomayor EM.
Division of Immunology, Department of Interdisciplinary Oncology, H.
Lee Moffitt Cancer Center & Research Institute, University of South
Florida, Tampa, FL 33612, USA.
Toll-like receptors (TLR) expressed by cells of the immune system play
a central role in the generation of immune responses against
pathogens. Following TLR ligation, both pro-inflammatory and anti-
inflammatory mediators are produced in order to elicit an immune
response that controls the microbial infection while limiting tissue
damage. Among these mediators, the pro-inflammatory cytokine IL-12 and
the anti-inflammatory cytokine IL-10 are known to play major roles.
Here, we show that in vitro or in vivo stimulation with flagellin, the
TLR5 ligand, does not result in IL-10 production. Furthermore,
flagellin inhibits IL-10 production by other specific TLR ligands at
the protein and mRNA levels while increasing IL-12p70 production.
Several studies have linked the activation of extracellular signal-
regulated kinases with IL-10 induction by TLR. We have observed that
LPS-induced extracellular signal-regulated kinase activation was
significantly decreased in flagellin-treated macrophages, suggesting
that this pathway might play a role in the inhibition of IL-10
production observed in flagellin-treated macrophages. Flagellin-
mediated IL-10 inhibition was not observed in cells that do not
express TLR5, supporting that this effect is indeed TLR5-dependent.
This study provides a new insight into the role of flagellin
recognition by TLR5 in shaping the immune response elicited by
flagellated microorganisms.
PMID: 17948265
------------
But what does what to make Th1 or th2?
Epidermal Langerhans Cells Rapidly Capture and Present Antigens from C-
Type Lectin-Targeting Antibodies Deposited in the Dermis.
Flacher V, Tripp CH, Stoitzner P, Haid B, Ebner S, Del Frari B, Koch
F, Park CG, Steinman RM, Idoyaga J, Romani N.
Department of Dermatology and Venereology, Innsbruck Medical
University, Innsbruck, Austria.
Antigen-presenting cells can capture antigens that are deposited in
the skin, including vaccines given subcutaneously. These include
different dendritic cells (DCs) such as epidermal Langerhans cells
(LCs), dermal DCs, and dermal langerin(+) DCs. To evaluate access of
dermal antigens to skin DCs, we used mAb to two C-type lectin
endocytic receptors, DEC-205/CD205 and langerin/CD207. When applied to
murine and human skin explant cultures, these mAbs were efficiently
taken up by epidermal LCs. In addition, anti-DEC-205 targeted langerin
(+) CD103(+) and langerin(-) CD103(-) mouse dermal DCs. Unexpectedly,
intradermal injection of either mAb, but not isotype control, resulted
in strong and rapid labeling of LCs in situ, implying that large
molecules can diffuse through the basement membrane into the
epidermis. Epidermal LCs targeted in vivo by ovalbumin-coupled anti-
DEC-205 potently presented antigen to CD4(+) and CD8(+) T cells in
vitro. However, to our surprise, LCs targeted through langerin were
unable to trigger T-cell proliferation. Thus, epidermal LCs have a
major function in uptake of lectin-binding antibodies under standard
vaccination conditions.Journal of Investigative Dermatology advance
online publication, 5 November 2009; doi:10.1038/jid.2009.343.
PMID: 19890348
Did i post this?
Must have. It's a rudensky and it means something. LOL
http://www.sciencemag.org/cgi/content/abstract/326/5955/986
CD4+ Regulatory T Cells Control TH17 Responses in a Stat3-Dependent
Manner
Ashutosh Chaudhry,1,2 Dipayan Rudra,1,2 Piper Treuting,3 Robert M.
Samstein,1 Yuqiong Liang,1 Arnold Kas,2 Alexander Y. Rudensky1,2,*
Distinct classes of protective immunity are guided by activation of
STAT transcription factor family members in response to environmental
cues. CD4+ regulatory T cells (Tregs) suppress excessive immune
responses, and their deficiency results in a lethal, multi-organ
autoimmune syndrome characterized by T helper 1 (TH1) and T helper 2
(TH2) CD4+ T cell–dominated lesions. Here we show that pathogenic TH17
responses in mice are also restrained by Tregs. This suppression was
lost upon Treg-specific ablation of Stat3, a transcription factor
critical for TH17 differentiation, and resulted in the development of
a fatal intestinal inflammation. These findings suggest that Tregs
adapt to their environment by engaging distinct effector response–
specific suppression modalities upon activation of STAT proteins that
direct the corresponding class of the immune response.
============
Have to get back on L. plantarum track...
Ok, but just make the rubes read the triPe. LOL
I know...i know the secrets to the universe and multi poem
are hidden there...
Who says there's NO THERE in there?
Not i... just once before i die.
I'm all over probiotics and IL-10 THEN. <W>
www.ncbi.nlm.nih.gov/pubmed/19817754
Clin Exp Allergy. 2009 Oct 7.
Lactic acid bacteria differ in their ability to induce functional
regulatory T cells in humans.
de Roock S, van Elk M, van Dijk ME, Timmerman HM, Rijkers GT, Prakken
BJ, Hoekstra MO, de Kleer IM.
The Department of Pediatric Immunology, University Medical Centre
Utrecht, Wilhemina Children's Hospital, Utrecht, The Netherlands.
Summary Background Trials with probiotic lactic acid bacteria have
yielded different results, which may be due to the strains used.
Lactobacilli and bifidobacteria are known to be potent modulators of
the immune system. The capacity of these bacteria used as probiotics
to influence both T helper type 1 (Th1)- and Th2-mediated diseases has
been shown before. However, the ability of strains to induce forkhead
box P3 (FOXP3(+)) expressing regulatory T cells has not yet been
investigated. Objective Test the inherent differences between strains
in their capacity to induce functional regulatory T cells in human
peripheral blood mononuclear cells (PBMC). Methods Human PBMC were co-
cultured in vitro with either Bifidobacterium lactis W51,
Lactobacillus acidophilus W55 or Lactobacillus plantarum W62 or an
Escherichia coli control strain. The percentage of FOXP3(+) cells, the
origin of the induced cells and the functionality of these cells were
assessed. Results Probiotic strains differ in their capacity to induce
regulatory T cells. FOXP3(+) cells were induced from CD25(-) cells and
were able to suppress effector T cells. Naturally occurring regulatory
T cells were not affected by co-culture with lactobacilli. IL-10
concentrations found in the supernatant showed a trend towards the
same differences between strains. Blockade of IL-10 did not influence
the up-regulation of FOXP3. No differences between lactic acid
bacteria were found in IL-17, IFN-gamma or IL-13. Conclusions Some
probiotic strains are potent inducers of regulatory cells, while
others are not. The clear differences between strains imply that an in
vitro characterization of probiotic strains before application is
recommended.
PMID: 19817754
I guess I have my work to raise foxp3 and IL-10 to balance the
inflammatory teeter totter towards Th2 and lower Th1, Th17, TNF, IFN
et al, ahead of me. :)
---------
Only 199 hits for [keywords: probiotic bacteria IL-10] on pubmed:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=probiotic+bacteria+iL-10&log$=activity
Adding in keyword: lactobacillus (lowers the count to 123)
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=probiotic+bacteria+iL-10+lactobacillus&log$=activity
Here's one i should peruse:
www.ncbi.nlm.nih.gov/pubmed/19748696
Int J Food Microbiol. 2009 Oct 31;135(2):90-8. Epub 2009 Aug 26.
In vitro evaluation of Lactobacillus plantarum DSMZ 12028 as a
probiotic: emphasis on innate immunity.
Cammarota M, De Rosa M, Stellavato A, Lamberti M, Marzaioli I,
Giuliano M.
Department of Experimental Medicine, Biotechnology and Molecular
Biology Section, Medical School, Second University of Naples, Italy.
In this study, we analyzed the probiotic potential of L. plantarum
DSMZ 12028 in vitro using the pathogen E. coli K4 and a certified
probiotic, L. paracasei F19, as controls. Adhesion to intestinal
epithelial cells was evaluated using two cell lines, CaCo-2 and HT-29,
through the plate dilution method. Moreover, the bacteria/epithelial
dynamic interaction was continuously monitored using time-lapse
microscopy. Expression of the innate immunity receptors, the TLRs, was
evaluated by semi-quantitative PCR on an epithelial/bacteria co-
culture. Real-time PCR was used to monitor expression of TLRs and
cytokines in a monocytic cell line (THP-1) following bacterial
exposure. The adherence of the strain to intestinal epithelial cells
was comparable to that of the probiotic. Time-lapse experiments showed
that E. coli K4 induced cell death while L. plantarum did not affect
proliferation at a 10:1 bacteria/cell ratio. L. plantarum down-
regulated TLR mRNAs with the exception of TLR2, while L. paracasei F19
and E. coli K4 caused a significant (p<0.05) up-regulation of TLR2 and
4, respectively. To simulate the activation of underlying immune cells
in the lamina propria, we analyzed the immunomodulation of L.
plantarum on a monocytic cell line, THP-1. Proinflammatory cytokines,
such as TNFalpha, were increased by the presence of bacteria. The
pathogen E. coli K4 also induced a strong up-regulation of
proinflammatory cytokines, such as IL8, IL1beta and IL23. No
differences were observed between experimental groups for IFNgamma,
IL-10 and IL12p40. Overall, L. plantarum DSMZ 12028 demonstrated
probiotic traits, inducing a proinflammatory response just above the
"threshold level", which could prevent an inflammatory outcome, while
inducing a higher state of alertness in the defense system of the host
intestinal epithelial cells.
PMID: 19748696
Need to do the implant again--> butt wit L. Plantarum in the mix. :)
http://www.thewholewhey.com/3601/162253.html
Good gack over these ten hits for wit kit with kyo and me?
And let's pare down those 123 to 13 with plantarum?
================
Drinking a glass of red wine or eating some resveratrol does HELP.
Help what?
ncrease your sirtuin levels.
http://www.eurekalert.org/pub_releases/2009-12/miot-ssl121009.php
Study strengthens link between sirtuins and life extension
CAMBRIDGE, Mass. — A new paper from MIT biology professor Leonard
Guarente strengthens the link between longevity proteins called
sirtuins and the lifespan-extending effects of calorie restriction.
For decades, it has been known that cutting normal calorie consumption
by 30 to 40 percent can boost lifespan and improve overall health in
animals such as worms and mice. Guarente believes that those effects
are controlled by sirtuins — proteins that keep cells alive and
healthy in the face of stress by coordinating a variety of hormonal
networks, regulatory proteins and other genes.
In his latest work, published Dec. 15 in the journal Genes and
Development, Guarente adds to his case by reporting that sirtuins
bring about the effects of calorie restriction on a brain system,
known as the somatotropic signaling axis, that controls growth and
influences lifespan length.
"This puts SIRT1 at a nexus connecting the effects of diet and the
somatropic signaling axis," says Guarente. "This is a major shot
across the bow that says sirtuins really are involved in fundamental
aspects of calorie restriction."
Guarente and others believe that drugs that boost sirtuin production
could help fight diseases of aging such as diabetes and Alzheimer's,
improving health in later life and potentially extending lifespan.
Drugs that promote sirtuin production are now in clinical trials in
diabetes patients, with results expected next year.
How they did it: The researchers genetically engineered mice whose
ability to produce the major mammalian sirtuin SIRT1 in the brain was
greatly reduced. Those mice and normal mice were placed on a calorie-
restricted diet. The normal mice showed much lower levels of
circulating growth hormones, demonstrating that their somatotropic
signaling system was impaired, but calorie restriction had no effect
on hormone levels of mice that could not produce SIRT1.
Next steps: In future work, Guarente plans to investigate the
mechanism by which sirtuins regulate the somatotropic axis. The work
could also help researchers and companies in their search for small
molecules that modulate sirtuins for maximum benefit.
<sniP>
=============
http://www.lef.org/newsletter/2009/1215_Curcumin-Bioperine-Target-Breast-Cancer-Stem-Cells.htm
Curcumin and bioperine target breast cancer stem cells
[...]
The report is the first to conclude that curcumin and bioperine could
help prevent cancer by targeting stem cells. This mechanism has the
potential to prevent estrogen-sensitive tumors as well as more
aggressive non-estrogen dependent cancers.
“If we can limit the number of stem cells, we can limit the number of
cells with potential to form tumors,” Dr Kakarala noted. “Women at
high risk of breast cancer right now can choose to take the drugs
tamoxifen or raloxifene for prevention, but most women won’t take
these drugs because there is too much toxicity. The concept that
dietary compounds can help is attractive, and curcumin and piperine
appear to have very low toxicity.”
<sniP>
===========
randall... time out. Forgot to say it's kimchi time/ L. Plantarum