Th1/Th2

[Guest guest]

I think people shouldn't think in absolutes when describing TH1

and TH2 repones. In fact (and I'm going to quote from NATURE

page 260 July 2004 issue) cuz it's not that simple,

and I think in chronic inflammatory conditions, there's most likely

a shift back and forth between the two.:

*QUOTE: Differences in the signalling pathways that enforce TH1-TH2

differentiation, not to mention the ulitmate cause of TH1 or TH2

phenotype, remaian largely obscure "

END QUOTE.

To discuss these pathways as if the answers are 'known' by a

select few is .. well.. a joke really.

If we could control (or effectively shift) these reponses

effectively, then we could control sepsis (which is basically

an immune storm) and medicine still can't do that.

Remember in sepsis, alot of times the infection is brought under

control (or so they think) but the immune response is not.

Your last questions about Benicar/Mino is interesting.

And I don't know the answer.. but there's been enough people now on

high dose Benicar and low dose Mino to know SOMETHING's causing

adverse reactions, and in my opinion - I've never thought these

reactions were classical herxing. We really haven't gotten anywhere

coming close to answering what's going on with these people.

Barb

* reference quote:

" Inferences, questions and possibilities in toll-like receptor

signalling "

[in part]:

" IMO, here is the progression:

Acute infection--> chronic/occult infection -> chronic inflammation --

>

symptoms present as specific disorders depending on tissue type

(genetics, host-pathogen relationship) ---> secondary symptoms emerge

over time- allergies, GI problems, chemical and food sensitivities

etc. "

DURAMATER REPLIES:

I absolutely concur about your hypothesized progression, albeit not

from a scientific place but rather an experiential position.

What I'm particularly curious about is the Th1/Th2 relationship with

such a progression. I feel pretty confident in saying that in the

latest stage you hypothesize (allergies, chem & food sensitivities)

there is an over-regulation of Th2. But do we think there is a

concommitent up-regulation in Th1 (as hypothesized by whats his face)?

Or what is going on with Th1 if anything? From whence does the

inflammation arise?

And being new to the literature on Th1/Th2, please SOMEONE correct my

rudimentary knowledge if its wrong... My understanding is that as one

tries to, say, downregulate Th1, T cells are shifted to Th2. So (A)

can one have too much Th1 AND Th2? (seems like you can if just too

much

T cells are being generated in general) and ( lets say both are

being

over-done. If one tries to tamp down Th1 (in the context of too high

Th1 & Th2), will that shift it over to EVEN MORE Th2????

Lastly, what happens to folks taking benicar/mino if it really does

tamp down Th1 cytokines but they already have too much Th2? Do Th2-

related symptoms get even worse?

Again, apologies for the rudimentary nature of these questions, but

I'm

just starting to work on my understanding of these areas involving

Th1/Th2 & cytokines.