Altered immune response to exercise in patients with CFS/ME: a systematic literature review

[osisposis]

@osisposis the theme of this thread is altered immunity in CFS after exercise. You will get more discussion on your postings if you start another thread instead of adding off topic research here

but it's not off topic and I wasn't looking for discussion.
this study on CFS found we have high C4a, what makes C4a high is low/deficiency or dysfunction of C1-Inh.
C4a causes mast cells to degranulate. this not only applies to WDB, environmental exposures play a role in many inflammatory diseases includeing CFS.

 

[osisposis]

factor B (BF) and complement component 2 (C2) genes
These two genes, along with genes encoding complement components 4A (C4A) and 4B (C4B), reside
in the major histocompatibility complex (MHC) class III region.

Front Biosci. 2001 Aug 1;6960-72.
Human MHC class III and IV genes and disease associations.
Gruen JR1, Weissman SM.
Author information
Abstract
http://www.ncbi.nlm.nih.gov/pubmed/11487469

Front Biosci. 2001 Aug 1;6914-26.
Genetic organization of the human MHC class III region.
Milner CM1, Campbell RD.
Author information
Abstract
http://www.ncbi.nlm.nih.gov/pubmed/11487476

 

[osisposis]

Angioedema

Angioedema can be caused by either mast cell degranulation or activation of the kallikrein-kinin cascade. In the former case, angioedema can be caused by allergic reactions caused by immunoglobulin E (IgE)-mediated hypersensitivity to foods or drugs that can also result in acute urticaria or a more generalized anaphylactic reaction. Nonsteroidal anti-inflammatory drugs (cyclooxygenase 1 inhibitors, in particular) may cause angioedema with or without urticaria, and leukotrienes may have a particular role as a mediator of the swelling. Reactions to contrast agents resemble allergy with basophil and mast cell degranulation in the absence of specific IgE antibody and can be generalized, that is, anaphylactoid. Angioedema accompanies chronic urticaria in 40% of patients, and approximately half have an autoimmune mechanism in which there is IgG antibody directed to the subunit of the IgE receptor (40%) or to IgE itself (5%-10%). Bradykinin is the mediator of angioedema in hereditary angioedema types I and II (C1 inhibitor [INH] deficiency) and the newly described type III disorder some of which are caused by a mutation involving factor XII. Acquired C1 INH deficiency presents in a similar fashion to the hereditary disorder and is due either to C1 INH depletion by circulating immune complexes or to an IgG antibody directed to C1 INH. Although each of these causes excessive bradykinin formation because of activation of the plasma bradykinin-forming pathway, the angioedema due to angiotensin-converting enzyme inhibitors is caused by excessive bradykinin levels due to inhibition of bradykinin degradation. Idiopathic angioedema (ie, pathogenesis unknown) may be histaminergic, that is, caused by mast cell degranulation with histamine release, or nonhistaminergic. The mediator pathways in the latter case are yet to be defined. A minority may be associated with the same autoantibodies associated with chronic urticaria. Angioedema that is likely to be life threatening (laryngeal edema or tongue/pharyngeal edema that obstructs the airway) is seen in anaphylactic/anaphylactoid reactions and the disorders mediated by bradykinin. ..................

http://www.waojournal.org/content/1/6/103

http://www.waojournal.org/content/pdf/1939-4551-1-6-103.pdf

Acquired C1 inhibitor deficiency: Management and prognosis
http://www.uptodate.com/contents/acquired-c1-inhibitor-deficiency-management-and-prognosis

Serine proteases, their inhibitors and allergy
http://onlinelibrary.wiley.com/doi/10.1111/j.1398-9995.2006.01233.x/full


Allergy and immunology problems and musculoskeletal specialists - See more at: http://www.rheumatologynetwork.com/...culoskeletal-specialists#sthash.cBGiDMYa.dpuf



Increased vascular permeability in C1 inhibitor–deficient mice mediated by the bradykinin type 2 receptor
These data clearly indicate that the C1INH-deficient mice not only have increased vascular permeability, but also have an increased permeability response to an external irritant.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC150945/


Allergic diseases in the elderly

http://www.ncbi.nlm.nih.gov/pubmed/22409889

http://www.ctajournal.com/content/1/1/11

 

[osisposis]

in WDB exposures 3 things , complement, mast cells and oxidative stress stand out as playing major rollls

2014, Mast Cell Function
A New Vision of an Old Cell

http://jhc.sagepub.com/content/62/10/698.full.pdf+html



Immunol Res. 2006;34(2):157-76.
The role of complement in danger sensing and transmission.

http://www.ncbi.nlm.nih.gov/pubmed/16760575?dopt=Abstract




Circ Res. 2011 Jan 21;108(2):235-48. doi: 10.1161/CIRCRESAHA.110.223875.
Oxidation-specific epitopes are danger-associated molecular patterns recognized by pattern recognition receptors of innate immunity.


http://www.ncbi.nlm.nih.gov/pubmed/21252151?dopt=Abstract&holding=npg



2014,Oxidative post-translational modifications and their involvement in the pathogenesis of autoimmune diseases


http://www.ncbi.nlm.nih.gov/pubmed/24955328


http://www.sciencedirect.com/science/article/pii/S221323171400069X