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Joined: Jan 2004
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Very_Addicted_to_AS_Kickin
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Very_Addicted_to_AS_Kickin
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http://www.medicalnewstoday.com/articles/174327.php

Breakthrough On Causes Of Inflammatory Bowel Disease
17 Dec 2009

http://www.medicalnewstoday.com/articles/169329.php
New Tool To Accelerate Discovery Of Autoimmune Disease Mechanisms And Therapies
31 Oct 2009

Both studies refer to gut problems... My gastroenterologist in the UK used to say that the gut was a bigger controller of the human body than most people, incl those in the medical profession, realised. whistle


MollyC1i - Riding OutAS
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This is an interesting comment from the second article, Molly:

Moreover, different autoimmune diseases aggregate within a single family, suggesting they are caused by disruptions in common biological pathways.

I know one family where one sibling has RA, another has Crohns and the third has MS. I'm puzzled about this situation and the cases where one individual has several different autoimmune diseases. How do genetics play a role in this - particularly when we're talking about markers that are associated with one autoimmune disease but not others, like HLAB27.


Wendy

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Very_Addicted_to_AS_Kickin
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Like my cousins - One had MS, her sister had ?AS

My first DX was MS.

I am HLA-B27 negative, but have: AS, IBD, Psoriasis, Sjogren's, Reynauds - and that's just the autoimmune lot (goodness what else!) Depends how it is going to express?

My brother might have had AS, certainly had very bad neck and spine, then developed heart problems, Died in hospital with endocarditis .

Otherwise looks like the rest of the family are clear.


MollyC1i - Riding OutAS
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I seem to be the black sheep in my family in so many ways, being unique with regards to autoimmune diseases shouldn't surprise me. I know my mother had troubles with her bowels which required radical surgery (she would often say that half of her guts were taken out) but I never knew what exactly was wrong.

As for AS, there is nothing but the usual complaints of "bad backs". Then again, I never knew my father's side of the family, or him for that matter, so I wonder what sort of history might be found there? It's funny but this has never occurred to me before?

I think I need to write some letters.

Interesting.

Chris

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There's a clear pattern in my family, Chris, including a brother with identical, but slightly milder, symptoms to me. My grandmother had severe deforming RA, my father had bowel problems, I have another brother with celiac.


Wendy

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I have Crohn's and AS. Thankfully both don't flare at the same time.

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Humans have coevolved with microbial partners, and for the most part the interactions established can be considered positive or neutral. This is clearly the case of the flora composed of commensals and symbiotes that invade our lung skin or gut soon after birth. However, in some rare instances interactions with microorganisms can be detrimental and lead to pathological consequences. Despite these different outcomes, the distinction between a commensal and a pathogenic organism is not always obvious. For instance, Mycobacterium tuberculosis, present in two billion individuals worldwide, behaves more often as a commensal than a parasite. It is therefore not surprising that many of the strategies we have developed to coexist with our “positive” partners can be hijacked or manipulated by potentially harmful microorganisms to ensure their own survival. Indeed, many pathogens have evolved mechanisms to manipulate the regulatory network of the host to their advantage, thereby generating conditions that secure their survival for an extended period of time.
However, surviving an infection requires the generation of a controlled immune response in the host that recognises and controls the invading pathogen while limiting collateral damage to self tissues that may result from an overly exuberant immune response. This implies that induction of regulatory T cells (Treg’s) arises as a result of the host response to the infectious process in a bid to maintain or restore homeostasis.
If the regulatory process is too excessive (that is the immune system is overly suppressed) then the pathogen may be allowed to replicate without restraint overwhelming the host.
Immune responses in the context of infection can have varying effects on the potential development of autoimmunity. On the one hand pathogens, via Toll- like receptors and other mechanisms, can enhance immunosuppressive cells which can result in infection being negatively correlated with autoimmunity.
Rates of both allergy and autoimmunity are lower in developing countries where rates of infectious diseases are higher. There is a growing body of literature supporting the idea that microorganism persistence is in some cases necessary for the maintenance of protective immunity. For example, in Candida albicans infection in mice, reduction in the number of Treg’s leads to a better clearance of the primary infection, but is associated with a more damaging pathology as well as a loss of immunity to re-infection. These ideas underpin the notion of lessening the pathology associated with IBD by deliberately infecting the host with a hookworm. The immune response is redirected or skewed in a different direction by the new pathogen, thereby down-playing the damaging effects of the original disease-associated pathogen.

Cheers David


Dx Oct 2006 B27+ undifferentiated spondlyarthropathy (uSpA) with mild sebhorrhoeic dermatitis and mild Inflammatory Bowel Disease (IBD) controlled by NSD since 2007.
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Very_Addicted_to_AS_Kickin
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Just remembered, my youngest bro has Meunieres disease. Also, bro has had colon polyps - did not amuse him, at all. (But then he is a doctor... alien)

And I also have that darn IBD, with stomach and colon polyps. No. Not much fun...

So, one way and another, there is quite a bit of autoimmune conditions in the family.


MollyC1i - Riding OutAS

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