Hypothetical model for lymphocyctes

[Guest guest]

Hi Barb.

Thanks for the feedback. Perhaps we can view suspressed Lymphocytes

as part of the effect of having undergone chronic systemic

inflammation?

Regarding the model, I think perhaps I've misled you with the term

lymphocyctes. I was thinking wider, perhaps even as wide to consider

all active motile cells (leukocyctes): monocyctes, macrophages,

dentritic, NKs, eosinophils, neutrophils, basophils, mast cells etc.

Does this fit better?

Best regards, .

>

> Hi .

> I checked your file.

> Pretty cool and probably correct in a healthy person, or if the

> infected person has robust ymphocytes.

>

>

> But what about in the cases of Lympocyte supression, which can

occur

> in some chronic cases?

>

> WHen I was on speaking terms with the MP.com (before there was an

> MP.com)alot of the respondents to the question of " show me your CBC

> data "

> had clear cases of supressed Lymps.

> Some of my blood tests showed >18K WBC count and under 10% were

> Lympocytes... clear supression of that class.

>

> Barb

>

>

>

>

> GARY wrote in part:

> The hypothesis is that dependent on their environment

> lymphocyctes

> are engaged towards achieving one of these three activities. Focus

> too far in any one direction leading to disease conditions.

[Guest guest]

YEP!!!

Baeb

wrote:

Hi Barb.

Thanks for the feedback. Perhaps we can view suspressed Lymphocytes

as part of the effect of having undergone chronic systemic

inflammation?

Regarding the model, I think perhaps I've misled you with the term

lymphocyctes. I was thinking wider, perhaps even as wide to consider

all active motile cells (leukocyctes): monocyctes, macrophages,

dentritic, NKs, eosinophils, neutrophils, basophils, mast cells etc.

Does this fit better?

Best regards, .

[Guest guest]

,

do you have your file avail in a format other than powerpoint? i'd

love to look at it, but don't have that program on the computer

available to me.

many thanks.

[Guest guest]

, they say the best solutions are sometimes the simplest solutions ...Could it be??? ..could this be the biggest breakthrough in unravelling the mysteries of infectious disease?....It makes perfect sense & as you know matches my history exactly...I didn't know introducing a pathogen has helped to kill cancers!! when you consider that it all falls into place ...You've already solved one deep mystery, explaining the chain reaction process of inflammation & how ARb's mop up that inflammation reducing the dependence on ARB's ...Add to that, the possibility that immune stimulants such as the cytokine Interleukin-2 .could prove to be the missing link ... To me it represents the best shot yet ...early days but , I feel privileged to receive the information ...thanks for being there...

-----Original Message-----From: garyrsmith36 [mailto:gary.smith@...]Sent: 30 March 2005 12:13infections Subject: [infections] Hypothetical model for lymphocyctesHi.I've posted a file which I would like you guys to review.In this three way model I have considered three main functions for lymphocyctes: Wound clearance (Inflammation), Wound resolution (healing) and pathogen recognition/killing.The hypothesis is that dependent on their environment lymphocyctes are engaged towards achieving one of these three activities. Focus too far in any one direction leading to disease conditions.Although perhaps not a precise analogy you could consider so called TH2 diseases at the top 'hypersensitivity' and on the bottom left TH1.Glucocorticoids block inflammation mediators, but they also block IL-2, hence Cushing's syndrome on the bottom right.Pathogens promote inflammation (some TH1 diseases) in order to avoid effective immune response. Regarding colds/flu and their effects on people suffering from TH1 we could imagine that initially you would feel worse due to the additional inflammation that the cold/flu causes. Once your system has recognised the virus however you start to generate additional IL-2 which takes your lymphocyctes away from inflammation and towards the top.This model also helps to explain something that puzzled me regarding cancer and that early treatment with an infecting agent helped to kill the cancers.I may have to delete this file in a day or so.Best regards, .

[Guest guest]

> Pathogens promote inflammation (some TH1 diseases) in order to avoid

> effective immune response.

Actually, they can do both. Parasites, such certain forms marlaria,

can induce TGF-Beta production, which then suppresses the TH1

response, and blocks the killing off of the parasites. Viruses, on

the other hand, such as EBV, prevent cells from responding to

TGF-Beta. TGF-Beta is important in bringing the TH1 response to a

resolution, so without TGF-Beta, the TH1 response (and inflammation)

continues, and the viruses survive.

Mark

[Guest guest]

Hi Mark.

A possibly unique attribute of the AT1 receptor is that it can

stimulate the expression of TGF-b. (TGF-b as well as being produced

by AT1 also circulates in the blood) TGF-b appears to play a

significant role both in wound clearance and wound resolution phases.

I would describe I think TGF-b as a key worker rather than a manager

of inflammation and healing.

In pathogen killing TGF-b plays a role too. In cancer for instance

TGF-b is part of the bodies initial defense mechanisms to promote

apoptosis in these faulty cells. Cancers seem to learn to avoid this

and other control systems through genetic changes as a prerequisite

for uncontrolled growth. I could see that certain virus's could also

be able to distrupt this process but then there are a number of

mechanisms for pathogen killing.

I think when we talk about messengers at the level of TGF-b we have

to careful to avoid absolutes since there is a very complex web of

messages going on. TGF-b may cause events in some environments and in

others it would contribute to something else. This is why I have been

trying to look at the endgames and the big picture in trying to model

what is going on. If I find the model doesn't fit then I'll puzzle

over it again.

Best regards, .

> > Pathogens promote inflammation (some TH1 diseases) in order to

avoid

> > effective immune response.

>

> Actually, they can do both. Parasites, such certain forms marlaria,

> can induce TGF-Beta production, which then suppresses the TH1

> response, and blocks the killing off of the parasites. Viruses, on

> the other hand, such as EBV, prevent cells from responding to

> TGF-Beta. TGF-Beta is important in bringing the TH1 response to a

> resolution, so without TGF-Beta, the TH1 response (and inflammation)

> continues, and the viruses survive.

>

> Mark

[Guest guest]

Here is doc Kaisers:

http://www.cat.cc.md.us/courses/bio141/lecguide/index.html

You may well need to learn some basics first, elsewhere on the web.

I had alot of trouble making sense of doc K's at first. Even when I

started to dig it, I had to read every section over and over again.

C Janeway's immunology text is often cited as a lucid introduction

for college level bioscience students. I've only looked at it for a

few min but saw at least one theory stated as fact. It has alot of

diagrams and pics. I wasnt as impressed with it as I expected, but

then I do have kinda a negative attitude about everything

Not everything in doc K's and these books is 100% reliable. Even

s " Fundamental Immunology " , at 1700 pp, yields

significantly less knowledge than what you can get from really

digging the journal lit on a particular topic. And of course, new

knowledge accretes really fast.

If you have any particular questions just ask, its no sweat for me

to fire off an answer cause I got it all swirling around in my head

already - will probably cost me all of 2 mintues.

Marie Mayberry <msmabrry@y...> wrote:

> I really want to learn about the immune system-at

> least I assume this is what this talk is about-but I

> really wish someone could draw me some pictures. I

> learn better that way, I am good at art but boy I

> don't have the background for this scientific stuff. I

> feel I need to do my own research but it is sooooo

> over my head.

> Anyone else relate?

[Guest guest]

Thanks ,

Whew, that is a lot of reading. It will take me some

time to plod through some of it. It does give me a

little background info though.

Marie

--- Hodologica <usenethod@...> wrote:

>

> Here is doc Kaisers:

>

>

http://www.cat.cc.md.us/courses/bio141/lecguide/index.html

>

>

> You may well need to learn some basics first,

> elsewhere on the web.

> I had alot of trouble making sense of doc K's at

> first. Even when I

> started to dig it, I had to read every section over

> and over again.

>

> C Janeway's immunology text is often cited as a

> lucid introduction

> for college level bioscience students. I've only

> looked at it for a

> few min but saw at least one theory stated as fact.

> It has alot of

> diagrams and pics. I wasnt as impressed with it as I

> expected, but

> then I do have kinda a negative attitude about

> everything

>

> Not everything in doc K's and these books is 100%

> reliable. Even

> s " Fundamental Immunology " , at 1700 pp,

> yields

> significantly less knowledge than what you can get

> from really

> digging the journal lit on a particular topic. And

> of course, new

> knowledge accretes really fast.

>

> If you have any particular questions just ask, its

> no sweat for me

> to fire off an answer cause I got it all swirling

> around in my head

> already - will probably cost me all of 2 mintues.

>

>

> Marie Mayberry <msmabrry@y...> wrote:

> > I really want to learn about the immune system-at

> > least I assume this is what this talk is about-but

> I

> > really wish someone could draw me some pictures. I

>

> > learn better that way, I am good at art but boy I

> > don't have the background for this scientific

> stuff. I

> > feel I need to do my own research but it is sooooo

>

> > over my head.

> > Anyone else relate?

>

>

>

>

>

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