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Dr. Federica Sallusto & Dr. Christina Zielinski -- Biomedicine and PSOR (and MORE) Disease Causation via Fungus (Candida vs Staph and Th2 critters) Foxp3- Tregs & IL10 vs Th17 & Th1 Skew in YOU
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randall
Apr 6, 2012, 12:29:53 PM4/6/12
to
hi
And the winner is..... for PSOR causation?
The winner is.... for PSOR onset?
No, no for causation.. ONLY right now..
That winner is FUNGUS....<see below>
LoL
Oh BOY.. is it the StaPh of life?
Like we would have missed it as it's so basic?
Or maybe only homeostatic?
Or all around us and like diet doesn't exPlain why
the other 97 to 98% of the poopulation doesn't GET IT.
Get it yet BB?
OK... but that fungi down below is low, like virals and
they can be a pain in the yOU KNOW WHAT.
What?
In your DNA or life or death or or or...the black death?
No that is a bug...
ok like hiv...
done..with it...
AND
Microflora are different from Microbiota how?
And how about enterotypes?
Is it good/bad microbiota/microflora versus which enterotypes?
And which does the gut trip that trips ill HEALTH and becomes
Mazmanian's pathobionts?
running with enterotypes ....and gut bugs... scary...
4 hits: enterotypes - pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=enterotypes
11247 hits: microflora - pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=microflora
6697 hits: microbiota - pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=microbiota
And they all live right under our nostrils but our animals
(dogs/cats etc) know us more by them then we DO..or ido, youDO?
Gi track Voodoo?
who do?
Christina Z do...
Dr. Christina Zielinski Biomedicine is who do?
Or figured out how IL1β switched from..
just read it..
http://www.sciencedaily.com/releases/2012/04/120405075223.htm
Microflora Have Decisive Role With Autoimmune Illnesses, Some Good,
Some Bad
------
http://www.sciencedaily.com/images/2012/04/120405075223.jpg
Psoriasis. When the right microorganisms are at work, immune cells
involved in the development of autoimmune illnesses like psoriasis,
multiple sclerosis and arthritis, can develop anti-inflammatory
properties. Particular fungi activate the immune cells involved in the
development of certain illnesses, whereas other microorganisms, in
particular bacteria that are found naturally on our skin, lend an anti-
inflammatory function to them. (Credit: © quayside / Fotolia)
-----
ScienceDaily (Apr. 5, 2012) — When the right microorganisms are at
work, immune cells involved in the development of autoimmune illnesses
like psoriasis, multiple sclerosis and arthritis, can develop anti-
inflammatory properties. Scientists at Charité -- Universitätsmedizin
Berlin and the Institute for Research in Biomedicine, Bellinzona,
Switzerland, have now made this discovery. The scientists have
demonstrated that particular fungi activate the immune cells involved
in the development of certain illnesses, whereas other microorganisms,
in particular bacteria that are found naturally on our skin, lend an
anti-inflammatory function to them
"This not only demonstrates that the composition of our microflora has
a decisive role in the development of chronic illnesses, but also that
the key cells causing illness can develop an anti-inflammatory
'twin'," explained Dr. Christina Zielinski, first author of the study.
Their work is published in the current issue of the scientific journal
Nature.
The 32-year old researcher from the Dermatology and Allergology Clinic
at Charité and Berlin-Brandenburg School for Regenerative Therapies,
and her colleagues identified the basic signals that contribute to
whether or not a pathogenic or anti-inflammatory immune cell develops.
It then emerged that interleukin 1b, one of the body's own immune
system hormones, works like a molecular switch. Its presence trains
immune cells during autoimmune occurrences to function destructively
and to release inflammatory messenger substances. Its absence, on the
other hand, allows the immune cells to mature into anti-inflammatory
counterparts. Interestingly, it is our own body's microorganisms that
decide whether interleukin 1b is produced and therefore which mode is
selected.
This observation prompted the scientists to also look for patients
suffering from an overproduction of interleukin 1b, which is the case
in the so-called auto-inflammatory syndromes (e.g. CAPS, Muckle-Wells,
or Schnitzler Syndromes). These patients, especially children, suffer
from multiple symptoms like fever, arthritis, and skin rashes. The
exact development of these diseases is, however, to a large extent
unexplained. Researchers tested whether a therapy of antibodies that
block interleukin 1b can generate anti-inflammatory potential in the
immune cells. In fact, after the introduction of this therapy the
immune cells produced inflammation-retardant messengers. They even
developed a memory to release the messenger substances over long time
periods.
"I am convinced that an imbalance in our microbial microflora has a
decisive influence on the development of chronic inflammatory
illnesses like rheumatism, Morbus Crohn and psoriasis. Our organism is
composed of ten times more microbial cells than our body's own cells.
Keeping this in check is not easy. Interleukin 1b is now turning out
to be a decisive molecular switch, which the microbes use to dictate
between healthy or sick," says Dr. Christina Zielinski. She sees great
potential in the therapy of inflammatory diseases by blocking this
messenger substance. In contrast to other immune therapies this does
not lead to a weakening of the immune system, but rather enables the
cells instead to be anti-inflammatory if needed, without losing the
ability to fight dangerous pathogens.
<snip>
OK i've only said the ratio of good to bad bugs in the colon are key
(pH wise) and then
went postal on SFB in the small instestine upon Dan Littman's/Ivanov
SFB inducts Th17 etc.
So
If this is HER then only four hits and not the money one(?)... the
above hit :(
4 hits - "Zielinski CE"[Author] - pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Zielinski%20CE%22%5BAuthor%5D
#1 of 4 does have those gut players like Th17 and bugs versus ROR-γt.
OK so it is the money hit...duh... i'm so dumb dumb. AND As Z only has
4 hits i'm discounting her DISCOVERY... maybe Z stands on the BACKs of
the GIANTS like Littman and Mazmanian and a zillion others with
mothers no doubt...
http://www.ncbi.nlm.nih.gov/pubmed/22466287
Nature. 2012 Apr 1. doi: 10.1038/nature10957.
Pathogen-induced human T(H)17 cells produce IFN-γ or IL-10 and are
regulated by IL-1β
Zielinski CE, Mele F, Aschenbrenner D, Jarrossay D, Ronchi F, Gattorno
M, Monticelli S, Lanzavecchia A, Sallusto F.
Source
Institute for Research in Biomedicine, Via Vincenzo Vela 6, 6500
Bellinzona, Switzerland.
Abstract
IL-17-producing CD4(+) T helper cells (T(H)17) have been extensively
investigated in mouse models of autoimmunity. However, the
requirements for differentiation and the properties of pathogen-
induced human T(H)17 cells remain poorly defined. Using an approach
that combines the in vitro priming of naive T cells with the ex vivo
analysis of memory T cells, we describe here two types of human T(H)17
cells with distinct effector function and differentiation
requirements. Candida albicans-specific T(H)17 cells produced IL-17
and IFN-γ, but no IL-10, whereas Staphylococcus aureus-specific T(H)17
cells produced IL-17 and could produce IL-10 upon restimulation. IL-6,
IL-23 and IL-1β contributed to T(H)17 differentiation induced by both
pathogens, but IL-1β was essential in C. albicans-induced T(H)17
differentiation to counteract the inhibitory activity of IL-12 and to
prime IL-17/IFN-γ double-producing cells. In addition, IL-1β inhibited
IL-10 production in differentiating and in memory T(H)17 cells,
whereas blockade of IL-1β in vivo led to increased IL-10 production by
memory T(H)17 cells. We also show that, after restimulation, T(H)17
cells transiently downregulated IL-17 production through a mechanism
that involved IL-2-induced activation of STAT5 and decreased
expression of ROR-γt. Taken together these findings demonstrate that
by eliciting different cytokines C. albicans and S. aureus prime
T(H)17 cells that produce either IFN-γ or IL-10, and identify IL-1β
and IL-2 as pro- and anti-inflammatory regulators of T(H)17 cells both
at priming and in the effector phase.
PMID: 22466287
So we need staph to lower psor via more foxp3--> IL-10 and more
TREGs? Give me the staph of CLEAR... LOL
#2 of 4
http://www.ncbi.nlm.nih.gov/pubmed/21349085
Immunol Rev. 2011 Mar;240(1):40-51. doi: 10.1111/j.1600-065X.
2010.01000.x.
Dissecting the human immunologic memory for pathogens.
Zielinski CE, Corti D, Mele F, Pinto D, Lanzavecchia A, Sallusto F.
Source
Institute for Research in Biomedicine, Bellinzona, Switzerland.
Abstract
Studies on immunologic memory in animal models and especially in the
human system are instrumental to identify mechanisms and correlates of
protection necessary for vaccine development. In this article, we
provide an overview of the cellular basis of immunologic memory. We
also describe experimental approaches based on high throughput cell
cultures, which we have developed to interrogate human memory T cells,
B cells, and plasma cells. We discuss how these approaches can provide
new tools and information for vaccine design, in a process that we
define as 'analytic vaccinology'.
PMID: 21349085
Z's #3 and 4 are along these lines but OLD now...
Let's go with Dr. Federica Sallusto
http://bsi.immunology.org/view.image?Id=1180
Now this is more like it... a giant for Z to stand on? LoL
Some info on FS
http://www.ssai-sgai.ch/index.php?id=35
162 hits - "Sallusto F"[Author]
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Sallusto%20F%22%5BAuthor%5D
#2 is a foxp3 (low for psor folks skewed via Th1/Th17 cells)
http://www.ncbi.nlm.nih.gov/pubmed/22438251
Blood. 2012 Mar 21.
Functionally distinct subsets of human FOXP3+ Treg cells that
phenotypically mirror effector TH cells.
Duhen T, Duhen R, Lanzavecchia A, Sallusto F, Campbell DJ.
Source
Benaroya Research Institute, Seattle, WA, United States;
Abstract
FOXP3(+) regulatory T (Treg) cells are a broadly acting and potent
anti-inflammatory population of CD4(+) T cells essential for
maintaining immune homeostasis and preventing debilitating
autoimmunity. Based on chemokine receptor expression, we identified
separable populations of Treg cells in human blood expected to co-
localize with different helper T (T(H)) cell subsets. Although each
population was functionally suppressive, they displayed unique
patterns of pro- and anti-inflammatory cytokine production,
differentially expressed lineage-specifying transcription factors, and
responded differently to antigens associated with T(H)1 and T(H)17
responses. These results highlight a previously unappreciated degree
of phenotypic and functional diversity in human Treg cells that allows
subsets with unique specificities and immunomodulatory functions to be
targeted to defined immune environments during different types of
inflammatory responses.
PMID: 22438251
OK so we have someone working for US... and giving us GOOD FACTs about
our pathways/condition.
Now..
How do they fix us cheaply and homeostatically?
WE want it... lol
Is it lower SFB via L. Plantarum and then raise the acidity of the
colon
via lactic acid loving bacteria?
Slightly acidic colons are a birth right so don't kill the good ones
with antibiotic bugs/drugs.
From funky soil like easter island or norway or dumbo way...
and then EAT some sweet whey to keep them good ones happy 24/7 the
rest of your life any way...
randall... i guess i could come up with more....but not RIGHT
now...after i re read what is writ.
And the winner is..... for PSOR causation?
The winner is.... for PSOR onset?
No, no for causation.. ONLY right now..
That winner is FUNGUS....<see below>
LoL
Oh BOY.. is it the StaPh of life?
Like we would have missed it as it's so basic?
Or maybe only homeostatic?
Or all around us and like diet doesn't exPlain why
the other 97 to 98% of the poopulation doesn't GET IT.
Get it yet BB?
OK... but that fungi down below is low, like virals and
they can be a pain in the yOU KNOW WHAT.
What?
In your DNA or life or death or or or...the black death?
No that is a bug...
ok like hiv...
done..with it...
AND
Microflora are different from Microbiota how?
And how about enterotypes?
Is it good/bad microbiota/microflora versus which enterotypes?
And which does the gut trip that trips ill HEALTH and becomes
Mazmanian's pathobionts?
running with enterotypes ....and gut bugs... scary...
4 hits: enterotypes - pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=enterotypes
11247 hits: microflora - pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=microflora
6697 hits: microbiota - pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=microbiota
And they all live right under our nostrils but our animals
(dogs/cats etc) know us more by them then we DO..or ido, youDO?
Gi track Voodoo?
who do?
Christina Z do...
Dr. Christina Zielinski Biomedicine is who do?
Or figured out how IL1β switched from..
just read it..
http://www.sciencedaily.com/releases/2012/04/120405075223.htm
Microflora Have Decisive Role With Autoimmune Illnesses, Some Good,
Some Bad
------
http://www.sciencedaily.com/images/2012/04/120405075223.jpg
Psoriasis. When the right microorganisms are at work, immune cells
involved in the development of autoimmune illnesses like psoriasis,
multiple sclerosis and arthritis, can develop anti-inflammatory
properties. Particular fungi activate the immune cells involved in the
development of certain illnesses, whereas other microorganisms, in
particular bacteria that are found naturally on our skin, lend an anti-
inflammatory function to them. (Credit: © quayside / Fotolia)
-----
ScienceDaily (Apr. 5, 2012) — When the right microorganisms are at
work, immune cells involved in the development of autoimmune illnesses
like psoriasis, multiple sclerosis and arthritis, can develop anti-
inflammatory properties. Scientists at Charité -- Universitätsmedizin
Berlin and the Institute for Research in Biomedicine, Bellinzona,
Switzerland, have now made this discovery. The scientists have
demonstrated that particular fungi activate the immune cells involved
in the development of certain illnesses, whereas other microorganisms,
in particular bacteria that are found naturally on our skin, lend an
anti-inflammatory function to them
"This not only demonstrates that the composition of our microflora has
a decisive role in the development of chronic illnesses, but also that
the key cells causing illness can develop an anti-inflammatory
'twin'," explained Dr. Christina Zielinski, first author of the study.
Their work is published in the current issue of the scientific journal
Nature.
The 32-year old researcher from the Dermatology and Allergology Clinic
at Charité and Berlin-Brandenburg School for Regenerative Therapies,
and her colleagues identified the basic signals that contribute to
whether or not a pathogenic or anti-inflammatory immune cell develops.
It then emerged that interleukin 1b, one of the body's own immune
system hormones, works like a molecular switch. Its presence trains
immune cells during autoimmune occurrences to function destructively
and to release inflammatory messenger substances. Its absence, on the
other hand, allows the immune cells to mature into anti-inflammatory
counterparts. Interestingly, it is our own body's microorganisms that
decide whether interleukin 1b is produced and therefore which mode is
selected.
This observation prompted the scientists to also look for patients
suffering from an overproduction of interleukin 1b, which is the case
in the so-called auto-inflammatory syndromes (e.g. CAPS, Muckle-Wells,
or Schnitzler Syndromes). These patients, especially children, suffer
from multiple symptoms like fever, arthritis, and skin rashes. The
exact development of these diseases is, however, to a large extent
unexplained. Researchers tested whether a therapy of antibodies that
block interleukin 1b can generate anti-inflammatory potential in the
immune cells. In fact, after the introduction of this therapy the
immune cells produced inflammation-retardant messengers. They even
developed a memory to release the messenger substances over long time
periods.
"I am convinced that an imbalance in our microbial microflora has a
decisive influence on the development of chronic inflammatory
illnesses like rheumatism, Morbus Crohn and psoriasis. Our organism is
composed of ten times more microbial cells than our body's own cells.
Keeping this in check is not easy. Interleukin 1b is now turning out
to be a decisive molecular switch, which the microbes use to dictate
between healthy or sick," says Dr. Christina Zielinski. She sees great
potential in the therapy of inflammatory diseases by blocking this
messenger substance. In contrast to other immune therapies this does
not lead to a weakening of the immune system, but rather enables the
cells instead to be anti-inflammatory if needed, without losing the
ability to fight dangerous pathogens.
<snip>
OK i've only said the ratio of good to bad bugs in the colon are key
(pH wise) and then
went postal on SFB in the small instestine upon Dan Littman's/Ivanov
SFB inducts Th17 etc.
So
If this is HER then only four hits and not the money one(?)... the
above hit :(
4 hits - "Zielinski CE"[Author] - pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Zielinski%20CE%22%5BAuthor%5D
#1 of 4 does have those gut players like Th17 and bugs versus ROR-γt.
OK so it is the money hit...duh... i'm so dumb dumb. AND As Z only has
4 hits i'm discounting her DISCOVERY... maybe Z stands on the BACKs of
the GIANTS like Littman and Mazmanian and a zillion others with
mothers no doubt...
http://www.ncbi.nlm.nih.gov/pubmed/22466287
Nature. 2012 Apr 1. doi: 10.1038/nature10957.
Pathogen-induced human T(H)17 cells produce IFN-γ or IL-10 and are
regulated by IL-1β
Zielinski CE, Mele F, Aschenbrenner D, Jarrossay D, Ronchi F, Gattorno
M, Monticelli S, Lanzavecchia A, Sallusto F.
Source
Institute for Research in Biomedicine, Via Vincenzo Vela 6, 6500
Bellinzona, Switzerland.
Abstract
IL-17-producing CD4(+) T helper cells (T(H)17) have been extensively
investigated in mouse models of autoimmunity. However, the
requirements for differentiation and the properties of pathogen-
induced human T(H)17 cells remain poorly defined. Using an approach
that combines the in vitro priming of naive T cells with the ex vivo
analysis of memory T cells, we describe here two types of human T(H)17
cells with distinct effector function and differentiation
requirements. Candida albicans-specific T(H)17 cells produced IL-17
and IFN-γ, but no IL-10, whereas Staphylococcus aureus-specific T(H)17
cells produced IL-17 and could produce IL-10 upon restimulation. IL-6,
IL-23 and IL-1β contributed to T(H)17 differentiation induced by both
pathogens, but IL-1β was essential in C. albicans-induced T(H)17
differentiation to counteract the inhibitory activity of IL-12 and to
prime IL-17/IFN-γ double-producing cells. In addition, IL-1β inhibited
IL-10 production in differentiating and in memory T(H)17 cells,
whereas blockade of IL-1β in vivo led to increased IL-10 production by
memory T(H)17 cells. We also show that, after restimulation, T(H)17
cells transiently downregulated IL-17 production through a mechanism
that involved IL-2-induced activation of STAT5 and decreased
expression of ROR-γt. Taken together these findings demonstrate that
by eliciting different cytokines C. albicans and S. aureus prime
T(H)17 cells that produce either IFN-γ or IL-10, and identify IL-1β
and IL-2 as pro- and anti-inflammatory regulators of T(H)17 cells both
at priming and in the effector phase.
PMID: 22466287
So we need staph to lower psor via more foxp3--> IL-10 and more
TREGs? Give me the staph of CLEAR... LOL
#2 of 4
http://www.ncbi.nlm.nih.gov/pubmed/21349085
Immunol Rev. 2011 Mar;240(1):40-51. doi: 10.1111/j.1600-065X.
2010.01000.x.
Dissecting the human immunologic memory for pathogens.
Zielinski CE, Corti D, Mele F, Pinto D, Lanzavecchia A, Sallusto F.
Source
Institute for Research in Biomedicine, Bellinzona, Switzerland.
Abstract
Studies on immunologic memory in animal models and especially in the
human system are instrumental to identify mechanisms and correlates of
protection necessary for vaccine development. In this article, we
provide an overview of the cellular basis of immunologic memory. We
also describe experimental approaches based on high throughput cell
cultures, which we have developed to interrogate human memory T cells,
B cells, and plasma cells. We discuss how these approaches can provide
new tools and information for vaccine design, in a process that we
define as 'analytic vaccinology'.
PMID: 21349085
Z's #3 and 4 are along these lines but OLD now...
Let's go with Dr. Federica Sallusto
http://bsi.immunology.org/view.image?Id=1180
Now this is more like it... a giant for Z to stand on? LoL
Some info on FS
http://www.ssai-sgai.ch/index.php?id=35
162 hits - "Sallusto F"[Author]
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Sallusto%20F%22%5BAuthor%5D
#2 is a foxp3 (low for psor folks skewed via Th1/Th17 cells)
http://www.ncbi.nlm.nih.gov/pubmed/22438251
Blood. 2012 Mar 21.
Functionally distinct subsets of human FOXP3+ Treg cells that
phenotypically mirror effector TH cells.
Duhen T, Duhen R, Lanzavecchia A, Sallusto F, Campbell DJ.
Source
Benaroya Research Institute, Seattle, WA, United States;
Abstract
FOXP3(+) regulatory T (Treg) cells are a broadly acting and potent
anti-inflammatory population of CD4(+) T cells essential for
maintaining immune homeostasis and preventing debilitating
autoimmunity. Based on chemokine receptor expression, we identified
separable populations of Treg cells in human blood expected to co-
localize with different helper T (T(H)) cell subsets. Although each
population was functionally suppressive, they displayed unique
patterns of pro- and anti-inflammatory cytokine production,
differentially expressed lineage-specifying transcription factors, and
responded differently to antigens associated with T(H)1 and T(H)17
responses. These results highlight a previously unappreciated degree
of phenotypic and functional diversity in human Treg cells that allows
subsets with unique specificities and immunomodulatory functions to be
targeted to defined immune environments during different types of
inflammatory responses.
PMID: 22438251
OK so we have someone working for US... and giving us GOOD FACTs about
our pathways/condition.
Now..
How do they fix us cheaply and homeostatically?
WE want it... lol
Is it lower SFB via L. Plantarum and then raise the acidity of the
colon
via lactic acid loving bacteria?
Slightly acidic colons are a birth right so don't kill the good ones
with antibiotic bugs/drugs.
From funky soil like easter island or norway or dumbo way...
and then EAT some sweet whey to keep them good ones happy 24/7 the
rest of your life any way...
randall... i guess i could come up with more....but not RIGHT
now...after i re read what is writ.
Bohgosity BumaskiL
May 25, 2012, 10:40:10 PM5/25/12
to
On 2012-04-06 10:29 AM, randall wrote:
(...)
Some of us are more necessarily vejetarian and needing of fruit, no
coffee, and no nicotine than others. There might even be a
population of people who are sensitive to nightshades (other than
Tobacco and Halapaynyohz). I suspect that all of these jenetik kozez
you are pointing at are just shades and varieties of intolerance to
meat. Been farming cows for fifty jenerations? You probably hav the
jeenz for eating saturated fat without getting atherosclerosis, too.
Most of Pagano's failures are people who did not stick to hiz rejimen.
Regimen is superior to medicine.
--Voltaire
French author, humanist, rationalist, & satirist (1694 - 1778)
(...)
The tilt on this machine iz towards very expensive injections that
leave you prone to cancer, because they suppress your immune system,
starting with cyclosporine.
(...)
> Or all around us and like diet doesn't exPlain why
> the other 97 to 98% of the poopulation doesn't GET IT.
(...)
> the other 97 to 98% of the poopulation doesn't GET IT.
Some of us are more necessarily vejetarian and needing of fruit, no
coffee, and no nicotine than others. There might even be a
population of people who are sensitive to nightshades (other than
Tobacco and Halapaynyohz). I suspect that all of these jenetik kozez
you are pointing at are just shades and varieties of intolerance to
meat. Been farming cows for fifty jenerations? You probably hav the
jeenz for eating saturated fat without getting atherosclerosis, too.
Most of Pagano's failures are people who did not stick to hiz rejimen.
Regimen is superior to medicine.
--Voltaire
French author, humanist, rationalist, & satirist (1694 - 1778)
(...)
> How do they fix us cheaply and homeostatically?
(...)
The tilt on this machine iz towards very expensive injections that
leave you prone to cancer, because they suppress your immune system,
starting with cyclosporine.
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