Simple & Effective --> Autoimmune Treatment --> with a IV Shot of IL-5 --> How Come they Didn't COME uP with THIS SOONER?

[randall]

hi



Pass me the IL-5 needle SHOT please!

Would that be in the BUTT bob?

http://en.wikipedia.org/wiki/Intravenous_therapy#Hypodermic_needle

No Mister Eubanks... it would NOT... LOL


How often does one need to shoot up?

And will it depend on severity?

And will JXR be able to do a LOW DOSE shot of IL-5?

And can we make it ourselves?

Do we want to make it OUR selves?

And why not a shot of IL-10 or foxp3 for that matter?

Or a shot of TREGs?

All of those will balance the Th1 skew of autoimmunity, RIGHT?


i dunno! Why or why not other they it's theory in my brain for a LONG
time... now.

And for people with CANCER and HIV/Aids certainly a shot of TNF and
IFN and
or the cytokines that spur such (Th17 etc) would be the reverse of
this autoimmune
treatment.

So?


Really?


OH.. here it is....


http://www.sciencedaily.com/releases/2012/05/120531102449.htm
'Simple and Effective' Injection Could Offer Hope for Treatment of
Autoimmune Disease

ScienceDaily (May 31, 2012) — Australian researchers have uncovered a
potential new way to regulate the body's natural immune response,
offering hope of a simple and effective treatment for auto-immune
diseases.

Auto-immune diseases result from an overactive immune response that
causes the body to attack itself.

The new approach involves increasing good regulating cells in the
body, unlike most current research which focuses on stopping "bad" or
"effector" cells, says lead researcher Dr Suzanne Hodgkinson, from
UNSW's Faculty of Medicine and Liverpool Hospital.

The researchers induced the body's T-cell front-line defences by
injecting cell-signalling proteins called cytokines, in particular
cytokine Interleukin-5 (II-5 cytokine).

When T-regulatory cells are grown in a way to make them specific to a
particular protein they develop receptors for the Il-5 cytokine. The
Il-5 cytokine boost allows the body's immune system to better regulate
its response to disease without going into overdrive.

The team cloned II-5 cytokine and injected it into rats with the
neurological condition Guillain-Barré syndrome. These rats recovered
much quicker and, if treated as a precaution, did not fall ill. The
method has also shown promise in animals with multiple sclerosis, with
kidney disease nephritis and trying to overcome organ transplantation
rejection.

"One of the nice things about this discovery is that it is one of the
few treatments in the auto-immune world and in the transplantation
world that works not by attacking the effector cells, but by
increasing the good regulating cells. So it works in a very different
way from almost every other treatment we've got available," Dr
Hodgkinson says.

Il-5 injections could be more palatable than inoculation by parasitic
worms -- another approach in regulating auto-immune conditions, the
researchers say.

International research shows swallowing helminths parasites can
regulate the immune system and boost T-cell production to combat
illnesses such as celiac disease and multiple sclerosis. The absence
of the worms in guts in the developed world has been cited as a
possible cause for the sharp rise in auto-immune diseases in Western
nations.

"The process we've developed may be the same process that the
helminths kick off. When you get a helminths infestation, one of the
changes in your immune response is an increase in cells called
eosinophils and these cells make the cytokine Interleukin-5," Dr
Hodgkinson says.

"In this new treatment, it's a matter of injecting the interleukin-5
and the body does the rest. It's both safe and effective and we think
inducing the immune response by injection may be more attractive to
people than swallowing parasitic worms."

The next step is to take the treatment to human trials, which could be
underway within two to five years, says Dr Hodgkinson, whose paper
outlining the study has been published in the journal Blood.

The research was supported by grants from Bob and Jack Ingham,
Liverpool Australia; Multiple Sclerosis Research Australia; the
Australian National Health and Medical Research Council; the Juvenile
Diabetes Research Foundation; Novatis; and funds from UNSW.

Lead researcher was UNSW research fellow Dr Giang Tran. Dr Hodgkinson
and co-author Professor Bruce Hall hold US patents related to the
treatment.
<snip>

Their abstract:

http://www.ncbi.nlm.nih.gov/pubmed/22310911
Blood. 2012 May 10;119(19):4441-50. Epub 2012 Feb 6.
IL-5 promotes induction of antigen-specific CD4+CD25+ T regulatory
cells that suppress autoimmunity.

Tran GT, Hodgkinson SJ, Carter NM, Verma ND, Plain KM, Boyd R,
Robinson CM, Nomura M, Killingsworth M, Hall BM.

Source
Immune Tolerance Laboratory, Faculty of Medicine, University of New
South Wales, Sydney, Australia; and.

Abstract
Immune responses to foreign and self-Ags can be controlled by
regulatory T cells (Tregs) expressing CD4 and IL-2Rα chain (CD25).
Defects in Tregs lead to autoimmunity, whereas induction of Ag-
specific CD4(+)CD25(+) Tregs restores tolerance. Ag-specific
CD4(+)CD25(+) FOXP3(+)Tregs activated by the T helper type 2 (Th2)
cytokine, IL-4, and specific alloantigen promote allograft tolerance.
These Tregs expressed the specific IL-5Rα and in the presence of IL-5
proliferate to specific but not third-party Ag. These findings suggest
that recombinant IL-5 (rIL-5) therapy may promote Ag-specific Tregs to
mediate tolerance. This study showed normal CD4(+)CD25(+) Tregs
cultured with IL-4 and an autoantigen expressed Il-5rα. Treatment of
experimental autoimmune neuritis with rIL-5 markedly reduced clinical
paralysis, weight loss, demyelination, and infiltration of CD4(+) (Th1
and Th17) CD8(+) T cells and macrophages in nerves. Clinical
improvement was associated with expansion of CD4(+)CD25(+)FOXP3(+)
Tregs that expressed Il-5rα and proliferated only to specific
autoantigen that was enhanced by rIL-5. Depletion of CD25(+) Tregs or
blocking of IL-4 abolished the benefits of rIL-5. Thus, rIL-5 promoted
Ag-specific Tregs, activated by autoantigen and IL-4, to control
autoimmunity. These findings may explain how Th2 responses, especially
to parasitic infestation, induce immune tolerance. rIL-5 therapy may
be able to induce Ag-specific tolerance in autoimmunity.

PMID: 22310911

While Tran has 22 hits some are aimed at this immune fix:

22 hits: Tran GT[Author]
http://www.ncbi.nlm.nih.gov/pubmed?term=Tran%20GT%5BAuthor%5D


~5 hits for : IL-5 - p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=IL-5&start=0&scoring=d&


http://en.wikipedia.org/wiki/Interleukin_5
Symbols IL5; EDF; IL-5; TRF
Interleukin 5 or IL-5 is an interleukin produced by T helper-2 cells
and mast cells. Its functions are to stimulate B cell growth and
increase immunoglobulin secretion. It is also a key mediator in
eosinophil activation. IL-5 is a 115-amino acid (in human, 133 in the
mouse) -long TH2 cytokine that is part of the hematopoietic family.
Unlike other members of this cytokine family (namely IL-3 and GM-
CSF) , this glycoprotein in its active form is a homodimer.[1] The
IL-5 gene is located on chromosome 11 (in the mouse, chromosome 5 in
humans) in close proximity to the genes encoding IL-3, IL-4, and
granulocyte-macrophage colony-stimulating factor (GM-CSF),[2][3] which
are often co-expressed in TH2 cells. Interleukin-5 is also expressed
by eosinophils [4] and has been observed in the mast cells of
asthmatic airways by immunohistochemistry.[5] IL-5 expression is
regulated by several transcription factors including GATA3.[6]
<snip>


43 hits - IL-5 + psoria*
http://www.ncbi.nlm.nih.gov/pubmed?term=psoria*%20IL-5

#1 of 43

http://www.ncbi.nlm.nih.gov/pubmed/21923616
Autoimmunity. 2012 Feb;45(1):44-54. Epub 2011 Sep 19.
The role of natural killer cells in autoimmune blistering diseases.

Zakka LR, Fradkov E, Keskin DB, Tabansky I, Stern JN, Ahmed AR.

Source
Center for Blistering Diseases, Boston, MA 02120, USA.

Abstract
The major focus of this paper is to describe and evaluate current
information on the role of natural killer cells (NK cells) in the
pathogenesis of blistering diseases. Until now, only pemphigus
vulgaris (PV) has been studied. One co-culture study demonstrated that
CD4+ T cells from the peripheral blood or perilesional skin of
patients with active disease proliferate and secrete cytokines in the
presence of major histocompatibility class II-expressing NK cells
loaded with antigenic desmoglein self-peptides. Another study showed
that NK cells can contribute to a T helper type 2-biased immune
response through impaired interleukins (IL)-12 signaling and
upregulation of IL, IL-10 and IL-5. Although significant data on other
blistering diseases are unavailable at present, some studies implicate
NK cells in disease progression. For instance, information on the role
of NK cells in psoriasis and their production of tumor necrosis factor-
α (TNF-α) will be provided since several TNF-α-inhibitors are used in
its treatment. Studies on alopecia areata are also included in this
paper because NK cells seem to play a key role in its pathogenesis.
This review highlights the potential importance of NK cells and NKT
cells as members of the large repertoire of cells and soluble
mediators that play a critical role in pathogenesis of blistering
diseases and other autoimmune diseases involving the skin. Therefore,
the authors advocate a greater focus and interest on the study of the
interaction of NK cells and the skin.

PMID: 21923616

#4 of 43

http://www.ncbi.nlm.nih.gov/pubmed/19622600
Evid Based Complement Alternat Med. 2011;2011:927294. Epub 2011 Jun
16.
The Role of Th17 in Neuroimmune Disorders: Target for CAM Therapy.
Part I.

Vojdani A, Lambert J.

Source
Immunosciences Lab., Inc., Los Angeles, CA 90035, USA.

Abstract
CD4(+) effector cells, based on cytokine production, nuclear receptors
and signaling pathways, have been categorized into four subsets. T-
helper-1 cells produce IFN-γ, TNF-β, lymphotoxin and IL-10; T-helper-2
cells produce IL-4, IL-5, IL-10, IL-13, IL-21 and IL-31; T-helper-3,
or regulatory T-cells, produce IL-10, TGF-β and IL-35; and the
recently discovered T-helper-17 cell produces IL-17, IL-17A, IL-17F,
IL-21, IL-26 and CCL20. By producing IL-17 and other signaling
molecules, Th17 contributes to the pathogenesis of multiple autoimmune
diseases including allergic inflammation, rheumatoid arthritis,
autoimmune gastritis, inflammatory bowel disease, psoriasis and
multiple sclerosis. In this article, we review the differential
regulation of inflammation in different tissues with a major emphasis
on enhancement of neuroinflammation by local production of IL-17 in
the brain. By understanding the role of pathogenic factors in the
induction of autoimmune diseases by Th17 cells, CAM practitioners will
be able to design CAM therapies targeting Th17 and associated cytokine
activities and signaling pathways to repair the intestinal and blood-
brain barriers for their patients with autoimmunities, in particular,
those with neuroinflammation and neurodegeneration.

PMID: 19622600
Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19622600/?tool=pubmed


Up chimP!.... don't be a Th2 chumP? LoL

How do we get more IL-5 without some phony drug or xyz?

We teach our microbiota to make it?

If only... <w>

9 hits - IL-5 + microbiota
http://www.ncbi.nlm.nih.gov/pubmed?term=IL-5%20microbiota

#1 has the white idea?


#1 of 9

http://www.ncbi.nlm.nih.gov/pubmed/21986357
Benef Microbes. 2011 Sep;2(3):183-92.
In vitro assessment of the immunomodulatory effects of multispecies
probiotic formulations for management of allergic diseases.

Rutten NB, Besseling-Van der Vaart I, Klein M, De Roock S, Vlieger AM,
Rijkers GT.

Source
Department of Pediatrics, University Medical Centre Utrecht, Utrecht,
the Netherlands.

Abstract
Modulation of the composition of the intestinal microbiota with
probiotics could possibly offer a way of prevention or management of
allergic diseases. The objective of this study was to determine the
immunomodulating effects of various multispecies probiotic
combinations in vitro, as preamble to application in vivo.
Multispecies probiotic combinations were formulated and tested for
their effects on in vitro cytokine production by human mononuclear
cells and were compared to products that already have shown beneficial
effects in vivo. All 4 tested combinations of probiotics showed a
40-71% decrease of Th2 cytokine production (IL-4, IL-5, and IL-13) and
a variable increase of Th1 (IFN-γ) and Treg cytokine (IL-10)
production compared to the medium. A specific probiotic mixture that
contained Bifidobacterium breve W25, Bifidobacterium lactis ATCC SD
5219, B. lactis ATCC SD 5220, Lactobacillus plantarum W62,
Lactobacillus salivarius W57 and Lactococcus lactis W19 was superior
in its stimulating effect on IL-10 production (significant better than
the other tested combinations; P=0.001). Modulation of in vitro
cytokine production profiles can be used to differentiate between
selected probiotic formulations for their immunomodulatory properties.
In the future it should be demonstrated whether the immunomodulatory
capacities from the multispecies probiotic formulation with the
desired profile will be effective in vivo (in adolescents, followed by
application in children).

PMID: 21986357

Can we MAKE the lactic acid loving bacteria pimP us some IL-5?


===============

BAck to BM Hall from top abstract: PMID: 22310911

http://www.ncbi.nlm.nih.gov/pubmed/18827184
Blood. 2009 Jan 8;113(2):479-87. Epub 2008 Sep 30.
CD4+CD25+ T cells alloactivated ex vivo by IL-2 or IL-4 become potent
alloantigen-specific inhibitors of rejection with different
phenotypes, suggesting separate pathways of activation by Th1 and Th2
responses.

Verma ND, Plain KM, Nomura M, Tran GT, Robinson C, Boyd R, Hodgkinson
SJ, Hall BM.

Source
Faculty of Medicine, University of New South Wales and Department of
Medicine, Liverpool Hospital, Liverpool, Australia.

Abstract
CD4(+)CD25(+)Foxp3(+) T cells are regulatory/suppressor cells (Tregs)
that include non-antigen (Ag)-specific as well as Ag-specific Tregs.
How non-Ag-specific naive CD4(+)CD25(+) Treg develop into specific
Tregs is unknown. Here, we generated adaptive Tregs by culture of
naive CD4(+)CD25(+)Foxp3(+) T cells with allo-Ag and either
interleukin-2 (IL-2) or IL-4. Within days, IL-2 enhanced interferon-
gamma receptor (Ifngammar) and Il-5 mRNA and IL-4 induced a reciprocal
profile with de novo IL-5Ralpha and increased IFN-gamma mRNA
expression. Both IL-2- and IL-4-alloactivated CD4(+)CD25(+) Tregs
within 3 to 4 days of culture had enhanced capacity to induce
tolerance to specific donor but not to third-party cardiac allografts.
These hosts became tolerant as allografts functioned more than 250
days, with a physiologic ratio of less than 10% CD4(+)CD25(+)Foxp3(+)
T cells in the CD4(+) population. CD4(+)CD25(+) T cells from tolerant
hosts given IL-2-cultured cells had increased Il-5 and Ifngammar mRNA.
Those from hosts given IL-4-cultured cells had enhanced IL-5Ralpha
mRNA expression and IL-5 enhanced their proliferation to donor but not
third-party allo-Ag. Thus, IL-2 and IL-4 activated allo-Ag-specific
Tregs with distinct phenotypes that were retained in vivo. These
findings suggested that T-helper 1 (Th1) and Th2 responses activate 2
pathways of adaptive Ag-specific Tregs that mediate tolerance. We
propose they be known as T-suppressor 1 (Ts1) and Ts2 cells.

PMID: 18827184
Free full text
http://bloodjournal.hematologylibrary.org/content/113/2/479.long

Hall has 3 tregs and 10 IL5 hits:
http://www.ncbi.nlm.nih.gov/pubmed?term=Hall%20BM%5BAuthor%5D%20IL-5

#2 of 10

http://www.ncbi.nlm.nih.gov/pubmed/19539571
Int Immunopharmacol. 2009 May;9(5):570-4. Epub 2009 Jan 29.
Alloantigen specific T regulatory cells in transplant tolerance.

Hall BM, Tran G, Hodgkinson SJ.

Source
Department of Medicine, The University of New South Wales, Liverpool
Hospital, Liverpool, NSW, Australia. b.h...@unsw.edu.au

Abstract
CD4(+)CD25(+)Foxp3(+)T cells are regulatory/suppressor cells (Treg)
that include non-antigen(Ag)-specific as well as Ag-specific Tregs.
How non-Ag-specific naïve CD4(+)CD25(+)Treg develop into specific
Tregs is unknown. We have studied DA rats tolerant to fully allogeneic
PVG cardiac grafts that survived with out immunosuppression for over
100 days and identified the cellular basis of alloantigen specific
tolerance. Key observations from our studies will be reviewed
including how CD4(+)CD25(+)Tregs were first identified and the
cytokine dependence of CD4(+)T cells that transfer alloantigen
specific transplant tolerance which died in culture unless stimulated
with both cytokine rich ConA supernatant and specific donor
alloantigen. Both the tolerant CD4(+)CD25(+) and CD4(+)CD25(-) T cell
populations are required to transfer tolerance, yet alone the
CD4(+)CD25(-) T cell effect rejection. Tolerance transfer occurs with
a low ratio of CD4(+)CD25(+)T cells (<1:10), whereas to induce
tolerance with naive CD4(+)CD25(+)T cells requires both a ratio of
>1:1 and is not alloantigen specific. Recent findings on how naïve
CD4(+)CD25(+)T cells developed into two separated pathways of
alloantigen specific Tregs, by culturing them with alloAg with either
IL-2 or IL-4 and donor alloantigen are described. IL-2 enhances IFN-
gammaR and IL-5 mRNA while IL-4 induced a reciprocal profile with de
novo IL-5Ralpha and increased IFN-gamma mRNA expression. Both IL-2 and
IL-4 alloactivated CD4(+)CD25(+)Tregs within 3-4 days of culture can
induce alloantigen specific tolerance at ratios of 1:10. Long term,
CD4(+)CD25(+)T cells from tolerant hosts given IL-2 cultured cells
have increased IL-5 and IFN-gammaR mRNA; whereas hosts given IL-4
cultured cells had enhanced IL-5Ralpha mRNA expression and IL-5
enhanced their proliferation to donor but not third party alloAg.
These findings suggest that Th1 and Th2 responses activate two
pathways of alloantigen specific Tregs that can mediate transplant
tolerance but are dependent upon cytokines produced by ongoing Th1 and/
or Th2 immune responses.

PMID: 19539571


^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^


The rest of the iL-5 page:

http://en.wikipedia.org/wiki/Interleukin_5

[...] Clinical significance

Interleukin-5 has long been associated with the cause of several
allergic diseases including allergic rhinitis and asthma, wherein a
large increase in the number of circulating, airway tissue, and
induced sputum eosinophils have been observed.[7] Given the high
concordance of eosinophils and, in particular, allergic asthma
pathology, it has been widely speculated that eosinophils have an
important role in the pathology of this disease.[8]

The IL-5 Receptor

The IL-5 receptor (IL-5R) belongs to the type I cytokine receptor
family and is a heterodimer composed of two polypeptide chains, one α
subunit, which binds IL-5 and confers upon the receptor cytokine
specificity, and one β subunit, which contains the signal transduction
domains.

α-subunit
The IL-5Rα chain is exclusively expressed by eosinophils, some
basophils and murine B1 cells or B cell precursors.[9] Like many other
cytokine receptors, alternative splicing of the α-chain gene results
in expression of either a membrane bound or soluble form of the bα-
chain. The soluble form does not lead to signal transduction and
therefore has an antagonistic effect on IL-5 signaling. Both monomeric
forms of IL-5Rα are low affinity receptors, while dimerization with
the β-chain produces a high affinity receptor.[10] In either case, the
α-chain exclusively binds IL-5 and the intra-cellular portion of
IL-5Rα is associated with Janus kinase (JAK) 2, a protein tyrosine-
kinase essential in IL-5 signal transduction.[11][12]

β-subunit
The β-subunit of the IL-5 receptor is responsible for signal
transduction and contains several intracellular signaling domains.
Unlike the α-chain, the β-chain does not bind IL-5, is not specific to
this cytokine, and is expressed on practically all leukocytes. In
fact, the β-subunit of the IL-5 receptor is also found in IL-3 and GM-
CSF receptors where it is associated the IL-3Rα and GM-CSFRα subunits
respectively.[13] Therefore, it is known as the common β receptor or
βc. As with the IL-5Rα subunit, the β subunit’s cytoplasmic domain is
constitutively associated with JAK2,[14] as well as LYN,[15] another
tyrosine kinase, which are both essential for IL-5 signal transduction.
[16]

Effect of IL-5 on Eosinophils

Eosinophils are terminally differentiated granulocytes found in most
mammals. The principal role of these cells, in a healthy host, is the
elimination of antibody bound parasites through the release of
cytotoxic granule proteins.[17] Given that eosinophils are the primary
IL-5Rα-expressing cells, it is not surprising that this cell type
responds to IL-5. In fact, IL-5 was originally discovered as an
eosinophil colony-stimulating factor,[18] is a major regulator of
eosinophil accumulation in tissues, and can modulate eosinophil
behavior at every stage from maturation to survival.

Interactions

Interleukin 5 has been shown to interact with Interleukin 5 receptor
alpha subunit.[19][20][21]
<snip>

****************************

This p ng thread has PMID: 20218931 that might be applicable:
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/496c826fcd81d658?&q=PMID%3A+20218931+

[...] http://www.ncbi.nlm.nih.gov/pubmed/20218931
Expert Opin Ther Pat. 2010 Mar 11.
Itk inhibitors: a patent review.

Lo HY.

Boehringer Ingelheim Pharmaceuticals, Inc., 900 Ridgebury Rd,
Ridgefield, CT 06877, USA +1 203 798 4923 ; +1 203 791 6072 ; ho-
yin...@boehringer-ingelheim.com.

Importance of field: IL-2 inducible T-cell kinase (Itk) is a non-
receptor tyrosine kinase of the Tec family. It plays an important
role
in T cell signaling and the production of various pro-inflammatory
cytokines such as IL-2, IL-4,____ IL-5, ____ IL-10 and IL-13.
Inhibition of Itk
has been a target for the treatment of diseases related to
inflammation disorders such as psoriasis and allergic asthma. Rich
resources on the structural information for Itk made discovery of
novel selective Itk inhibitors blossom in the past decade. Areas
covered in this review: In this report, distinct structural classes
of
specific Itk inhibitors are summarized and their in vitro/in vivo
properties are discussed. What the reader will gain: A summary of 21
patents including 16 different chemical structure classes of Itk
inhibitors. The in vivo efficacies of some of the inhibitors in
animal
models are also discussed. Take home message: Although some of the
inhibitors show efficacy in different animal models, which implies
potential for therapeutic use in human, there is not yet a chemical
entity reported in clinical trials. The prospects for Itk inhibitors
will rely on the quality of the compound and the validity of the
target in patients within the selected therapeutic area.

PMID: 20218931


http://en.wikipedia.org/wiki/ITK_(gene)
IL2-inducible T-cell kinase, also known as ITK, is a protein which in
humans is encoded by the ITK gene.[1]

Function
This gene encodes an intracellular tyrosine kinase expressed in T-
cells. The protein is thought to play a role in T-cell proliferation
and differentiation.[2][3]

Structure
This protein contains the following domains, which are often found in
intracellular kinases:[4]
N-terminus – PH (pleckstrin homology domain)
BTK – Bruton's tyrosine kinase Cys-rich motif
SH3 – (Src homology 3)
SH2 – (Src homology 2)
C-terminus – tyrosine kinase, catalytic domain
<sniP>


REACTs with:
http://en.wikipedia.org/wiki/FYN

http://en.wikipedia.org/wiki/Linker_of_activated_T_cells

[...] Function
The protein encoded by this gene is phosphorylated by ZAP70/SYK
protein tyrosine kinases following activation of the T-cell antigen
receptor (TCR) signal transduction pathway. This transmembrane
protein
localizes to lipid rafts (also known as glycosphingolipid-enriched
microdomains or GEMs) and acts as a docking site for SH2 domain-
containing proteins.[3] Upon phosphorylation, this protein recruits
multiple adaptor proteins and downstream signaling molecules into
multimolecular signaling complexes located near the site of TCR
engagement.[2]
<snip>


http://en.wikipedia.org/wiki/PLCG1
http://en.wikipedia.org/wiki/Lymphocyte_cytosolic_protein_2
http://en.wikipedia.org/wiki/KHDRBS1
http://en.wikipedia.org/wiki/Wiskott-Aldrich_syndrome_protein
<plus others>

[JRStern]

On Sat, 2 Jun 2012 11:39:29 -0700 (PDT), randall <ranh...@aol.com>
wrote:

That is frickin' remarkable!

What do you think?

J.

[Bohgosity BumaskiL]

In response to:
http://www.sciencedaily.com/releases/2012/05/120531102449.htm

On 2012-06-03 1:55 PM, JRStern wrote:
>
> That is frickin' remarkable!
>
> What do you think?
>
> J.
>

It's probably not az robust az getting more sun, water, and
eksersize. That iz what happens in summer, when PASI scores
naturally go down.

[Bohgosity BumaskiL]

This:
http://www.sciencedaily.com/releases/2012/05/120531102449.htm
Jeneralizes this:
http://bloodjournal.hematologylibrary.org/content/119/19/4441

They jeneralized it in ways that are not safe, too. All of the
experimenters were in the department of neurology. The animals
being researched were neurologically impaired mice. I've never heard
of swallowing worms to treat psoriasis, either.

This: http://www.ncbi.nlm.nih.gov/pubmed/22420195 describes patients
who would undergo anti-helminthic therapy, that iz a worm purj.