and the point is, we dont have all the answers on immune function

[Guest guest]

truth is ,that theres no way a defence team could prove that our illness is not

possable, if they had to.

truely with all considered it's more possable than not.

new science is proveing it. so, while sticking with all the old and very

confuseing self/nonself beliefs of how the immune system functions and what is

considered a allergy vs. a toxin,

and knowing that mycotoxins present in the body the same route as other

allergens and theres a hudge difference between harmless and toxic. the blurr is

a big factor here. and all I see is those who haven't spent hours on hours

trying to make sence of it all, just go along with the same old thoughts on

allergy. playing right into defence hands. I spent alot of hours on this and

nothing made sence until I read the danger model.

------------------

The Biological Notion of Self and Non-self

http://plato.stanford.edu/entries/biology-self/

----------------------------------------

THE DANGER MODEL:DANGER SIGNAL

THE DANGER MODEL:RENEWED SENCE OF SELF/Polly Matzinger

http://www.direct-ms.org/pdf/ImmunologyGeneral/DangerModel.pdf

Polly Matzinger

http://cmmg.biosci.wayne.edu/asg/polly.html

http://users.telenet.be/nmertens/U11/IM2_immunology.htm

------------

Trichothecene Mycotoxins Activate Inflammatory Response in Human Macrophages.

In conclusion, our results indicate that human macrophages sense

trichothecene mycotoxins as a DANGER SIGNAL, which activates caspase-1, and

further enables the secretion of IL-1â and IL-18 from the LPS-primed cells.

http://www.jimmunol.org/cgi/content/abstract/182/10/6418

------------

Toll-Like Receptor Priming Sensitizes Macrophages to Proinflammatory Cytokine

Gene Induction by Deoxynivalenol and Other Toxicants

These findings suggest that a primary " DANGER SIGNAL " (Matzinger, 2002) might

reprogram a host's innate immune system and render it sensitive to secondary

signals by a toxicant. We hypothesized that macrophages might be critical

targets for reprogramming of the innate immune system to a toxicant-sensitive

state. The goal of this research was to test this hypothesis by determining

(1)if LPS priming via TLR4 in vitro can sensitize macrophages to DON-induced

proinflammatory gene expression,

(2) whether other TLR agonists are capable of

priming the macrophage response to DON, and

(3) whether LPS priming of macrophages enhances their responsiveness to other

toxicants known to induce proinflammatory gene expression. The results suggest

that priming of macrophages via multiple TLRs increases their sensitivity to

induction of inflammatory gene

expression by DON and that, in an analogous fashion, LPS priming via TLR4

increases sensitivity to other toxicants with diverse mechanisms of action.

http://toxsci.oxfordjournals.org/content/92/2/445.full

-----------------------------------

Macrophages and Inflammatory Mediators in Chemical Toxicity: A Battle of Forces

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2787782/?tool=pubmed

-------------

this is a good read on mast cell functions

http://www3.interscience.wiley.com/cgi-bin/fulltext/123563063/HTMLSTART

Along with DC, mast cells are well positioned to be one of the first cells of

the immune system to interact with environmental Ag, environmentally derived

toxins, or invading pathogens

But one thing is certain: evolution did not give us mast cells so that we can

eat a peanut and die.

Answering these questions will take time. It is already clear, however, that

mast cells have a much larger spectrum of potential roles in health and disease

than was thought only a short time ago, when interest focused mainly on their

role as effector cells in IgE-associated responses. Indeed, mast cells are

increasingly viewed as versatile effector and immunoregulatory cells that occupy

a critical position at the interface of innate and acquired immunity,

where,depending on circumstances that remain to be fully understood, mast cells

may either help to sustain and restore health or contribute to disease.