the allergy thing

[Guest guest]

well, I suppose it depends on what a person chooses to believe.

I can see where if one wants to look at the allergy side of this and

what could happen in a WDB, considering autoimmunity/molecular mimicry

considering they did show allergy to many molds they were exposed to,

one could prove a case of being harmed pretty bad through this route.

actually it's a whole lot easier to connect things like melyin sleath damage and

meningitis, infection.

on the other side is the danger model and CIRS, TE.

I can see how these could intertwine.

even self attacking self could be quite toxic to our system.

I do realize many dont show a IgE responce to molds after a WDB exposure but

some do.

[Guest guest]

just some interesting links that may play in the the allergy/autoimmunity side

of things.

Scientists Show Monoclonal Antibody Leads To Repair Of Myelin Sheath In

Laboratory Study Of Multiple Sclerosis

http://www.medicalnewstoday.com/articles/85935.php

2009 Mechanisms of Primary Axonal Damage in a Viral Model of Multiple Sclerosis

http://www.jneurosci.org/cgi/content/full/29/33/10272

ANTIBODY'S

http://medical-dictionary.thefreedictionary.com/Receptors%2c+ige

SPECIFIC IgE HYTEC 288

IgE-mediated downregulation of L-selectin (CD62L) on lymphocytes from asthmatic

patients

(non-immunotherapy [iT] asthmatic group)

increasing concentrations of anti-IgE Ab (Anti-IgE Receptor Antibody) induced

progressively greater loss of L-selectin

L-selectin shedding is known to be a major mechanism by which L-selectin density

on the plasma membrane is regulated after activation of lymphocytes.

The experiments described here provide the first evidence of a novel level of

regulation of L-selectin expression that involves the IgE signal. Specifically,

engagement with anti-IgE Ab was shown to result in a marked inhibition of

L-selectin surface density on peripheral blood lymphocytes. Moreover, loss of

L-selectin surface expression on lymphocytes was attributed to an increase in

L-selectin shedding from the plasma membrane.

http://onlinelibrary.wiley.com/doi/10.1034/j.1398-9995.2001.056002164.x/full

Neutrophil Adhesion to Fibrinogen and Fibrin Under Flow Conditions Is Diminished

by Activation and L-Selectin Shedding (VASCULITIS)

http://bloodjournal.hematologylibrary.org/cgi/content/full/89/6/2131

Anti-IgE for chronic asthma in adults and children

http://www2.cochrane.org/reviews/en/ab003559.html

Localizing a Control Region in the Pathway to Leukotriene C4

Secretion Following Stimulation of Human Basophils with

Anti-IgE Antibody1

http://www.jimmunol.org/cgi/reprint/167/12/7027.pdf

Two Regions of Down-Regulation in the IgE-Mediated Signaling Pathway in Human

Basophils

http://www.jimmunol.org/cgi/content/full/170/10/4914

>

> well, I suppose it depends on what a person chooses to believe.

> I can see where if one wants to look at the allergy side of this and

> what could happen in a WDB, considering autoimmunity/molecular mimicry

> considering they did show allergy to many molds they were exposed to,

> one could prove a case of being harmed pretty bad through this route.

> actually it's a whole lot easier to connect things like melyin sleath damage

and meningitis, infection.

>

> on the other side is the danger model and CIRS, TE.

>

> I can see how these could intertwine.

>

> even self attacking self could be quite toxic to our system.

>

> I do realize many dont show a IgE responce to molds after a WDB exposure but

some do.

>