TH1/TH2 question for all of the knowledgable people here

Lot of views, no comments. Has this been asked and answered, or does nobody have anything to add? Am I way off base in this way of thinking?

I realize that not everyone thinks all cases of UC are autoimmune, but I think mine is.

That's NOT to say that screwed up gut flora and leaky gut aren't a huge part of it...they are common in AI disease, too. Some even think causative...

Whatever I knew on th1/th2 was years ago and pretty much forget.

Anyhow this study says that in UC there is an atypical th2 response. Not much after 2011 on google.

Hope this helps a little.

Old Mike

http://www.hindawi.com/journals/ulcers/2011/391787/

this one concludes not a Th2 problem. 2012 info

https://www.ecco-ibd.eu/index.php/publications/congress-abstract-s/abstracts-2012/item/p037-is-ulc-2.html

 

Here is a brief summary on TH1 and TH2 from text books.

ME:
Part of the issue is that much is still not understood about the immune system, though it wouldn't appear that way. Every day it seems something new is learned or discovered or overturned.

Just about everything in this regards (the immune system and response) is wonky in IBD...

TEXTBOOKS:
TH1 typically being known as a response to intracellular pathogens (so stuff effecting us that has made it's way inside our cells) and TH2 a response to extracellular pathogens (so stuff that's ummm trying to infect us) - or floating around bothering us like allergy type things as well. Ultimately it's called cell mediated immunity (TH1) and humoral immunity (TH2).

TH1 response activates things like macrophages and CD8+ (killer T-cells) to basically come eat the infected cells and deal with the infection..

TH2 is the response that activates B cells and begins the whole antibody production thing. So this response marks extracellular pathogens and antigens for destruction and elimination.

TH1 also being thought to be part of the delayed type hypersensitivity - so autoimmune type responses as you mentioned.

One the arguments and even some research shows that aside from autoimmune, its possible intracellular pathogens are the real culprit. Neither viewpoint has been proven or disproven.

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TEXTBOOKS:

T-Bet is the Master regulator for TH1 polarizing cytokines (IL-12,IFN-y, IL-18) and effector cytokines IFN-y and TNF.

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ME Again:
I believe lack of a functional TH1 response in the past seems to show to be beneficial to IBD... which is interesting from either perspective (autoimmune or intracellular bacteria).

BUT at the same time lack of T-BET results in spontaneous and communicable colitis - Old Mike Posted that one a long time ago. That paper showed how important T-BET and TH1 response is in keeping control of all the bacteria (commensals) as the paper states. Here is that paper www.ncbi.nlm.nih.gov/pmc/articles/PMC2169385/

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How does all that help with your question or thoughts??? I don't think it does! But maybe it will help you when you're reading things....

The body itself is designed to keep all these things in check... a swing one way or the other causes problems - so yes, perhaps helping maintain the right balance is something to try, BUT how does one know what to do... no one does. But maybe with some experimentation and time you can notice or see a benefit in some symptoms. Like with the Grape Seed Oil... if it works or seems to help, just keep at it. What the heck, it's not like there's anything to loose really.

Post Edited (Canada Mark) : 9/13/2014 7:46:18 PM (GMT-6)

Could you share the citation connecting turmeric use to SNPs? We're not aware of any credible link, but we're always happy to learn something new and add it (to SNPedia) so it can help others in the future.

It's well known that there are plenty of ways to inhibit (or enhance) CYP1A2 activity; for a pretty good list, see http://en.wikipedia.org/wiki/CYP1A2. But these are primarily dietary factors, not genetic factors, and since CYP1A2 activity is known to show wide differences in activity between individuals, only some of which can be explained genetically, we wouldn't put a whole lot of faith in that rs72547513 connection.

A connection between rs6323 and turmeric seems even more tenuous, frankly. It is a change reported as Benign/Likely Benign in ClinVar, which isn't surprising since it is not a variation that changes the amino acid at this position of the MAO-A protein, and, it's a variant carried by around 20% of all Caucasians (and 70% of all Asians), so it's not rare at all.

No claim to be an expert on CYP metabolism! In reviewing this further, there's really isn't much more (published) to go on, but there are two theoretical studies that have generated hypotheses explaining why this variation causes a decrease in CYP1A2 activity (and we've updated the SNP record in SNPedia to mention them).

How do you respond to coffee (caffeine) compared to others? This might be the simplest way to know if you have significantly reduced CYP1A2 metabolism, since caffeine is primarily metabolized by CYP1A2. Slow metabolizers are likely to experience a greater coffee effect (and possibly higher blood pressure) over longer periods of time than people who's CYP1A2 breaks it down quicker.

One other thought: given how rare an AA genotype at rs72547513 is expected to be (maybe 1 in 100,000?), you and/or your healthcare providers should confirm your genotype by a clinically validated genetic test for CYP1A2 (or via CYP1A2 phenotyping, i.e. directly checking your overall CYP1A2 activity) - or was your original test actually clinically validated?

We'll keep quiet now so the thread can return to your interesting question about TH1/TH2 interactions!