B-cells involvement in EHS?

Although the area of inquiry is not new in itself, this research IS new--in the sense of 'current'.  IMO, considering that 'Electrical Hypersensitivity Syndrome' is so-designated (viz., included amongst other 'hypersensitivity syndromes'), it is not surprising that immune dysregulation and, specifically, B-cell involvement is likely to play a significant role in the pathogenesis/pathophysiology of the illness.  The research linked above is from Discover Magazine and concerns B-cell involvement in Chronic Fatigue Syndrome (also known as Chronic Fatigue Immune Dysfunction Syndrome) whose symptoms overlap with EHS to an considerable extent (to put it mildly).

http://discovermagazine.com/2013/may/01-are-b-cells-to-blame-for-chronic-fatigue-syndrome#.UahgKlKFHEl

A 'syndrome' is essentially a cluster or constellation of signs(Sx) and symptoms(sx) which falls short of the classification of 'disease' which traditionally requires knowledge of what is causing the condition to be bona fide 'disease'.  So EHS can exist within CFS or CFS can exist within EHS without a conceptual problem.

Note that the Merck Manual classifies Hypersensitivity Reactions as Type I, II, III & IV, with Type I being what's known as "atopy" (IgE mediated allergy).  All hypersensitivity reactions are considered 'allergy' but only Type I is called "atopy".  Type I hypersensitivity reactions comprise those reactions that are immediate or quick developing, whereas the others are not.

This stuff is of interest in considering EHS, non?


Here's a snippet:

 
Allergic and other hypersensitivity disorders are exaggerated or inappropriate immune reactions.
 
Classification
 
The Gell and Coombs classification delineates 4 types
of hypersensitivity reaction. Hypersensitivity disorders often involve
more than 1 type.
 
Type I:  Type I reactions (immediate hypersensitivity) are
IgE-mediated. Antigen binds to IgE (which is bound to tissue mast cells
and blood basophils), triggering release of preformed mediators (eg,
histamine, proteases, chemotactic factors) and synthesis of other
mediators (eg, prostaglandins, leukotrienes, platelet-activating factor, cytokines). These mediators cause vasodilation, increased capillary
permeability, mucus hypersecretion, smooth muscle spasm, and tissue
infiltration with eosinophils, type 2 helper T cells (TH2),
and other inflammatory cells. Type I reactions underlie atopic disorders (eg, allergic asthma, rhinitis, conjunctivitis) and latex and some food allergies.

http://www.merckmanuals.com/professional/immunology_allergic_disorders/allergic_and_other_hypersensitivity_disorders/overview_of_allergy_and_hypersensitivity.html

This is a rather 'old school' approach however...


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