Research!

[Palmyra]

Hello to the crowd, and best wishes to all!

I surf many sites related to vasculitis, and this just appeared today via a very nice man that suffers from AI vasculitis, that has previously affected his central nervous system. His name is Jim, and he posts an online reference to many things published about vasculitis.

His site is:Vasculitis-Education : Vasculitis Education (http://health.groups.yahoo.com/group/Vasculitis-Education/)

His most recent post that got me excited is:

The immunogenetic architectur... [Cold Spring Harb Perspect Biol. 2012] - PubMed - NCBI (http://www.ncbi.nlm.nih.gov/pubmed/22383754)

Marta, Sange....what do you think....not big on content, but it is headed in a positive direction, no?

Hugs,
Jane, mom of Alison

[Al]

I've seen this paper, Jane. It is very good, though it is not exactly a breakthrough, in that other research has said essentially the same thing. Yet it could get the creative juices stirring in some hot-shot researchers. The point is that many autoimmune diseases have a strong overall heritable component ("heritable" means only that there is some correlation to genetic factors, not that genes in any predictable way cause the disease in question). The interesting twist in this paper is that the authors posit in interaction of two or more weakly correlated genetic components to make the effect stronger. In any case, it is clear enough that gene regulation (which genes are turned on or off at any given time) is heavily modified by many disease processes, and this is true whether the actual trigger is microbial or some environmental toxin. (Once the disease is doing its thing, it can be re-triggered, gene regulation can be modified, by other mechanisms, such as stress and physical trauma.)

Al

[pberggren1]

Thanks Jane. This is very interesting for sure.

[flana]

In plain english, anyone?

[Al]

In plain english, anyone? I'm assuming, Raj, that you are asking about my post, since I wrote the longest one. So...where do we start? What do you know now about ANCA diseases? How much do you want to know?

Al

[flana]

Had heard some research being conducted to identify markers in genes that identify WG activity, in the past, mostly from a doc at stanfords... is thos paper related to that? What is ANCO?

[Al]

Had heard some research being conducted to identify markers in genes that identify WG activity, in the past, mostly from a doc at stanfords... is thos paper related to that? What is ANCO? ANCO is a typo, Raj (for ANCA). I have fixed it now so as not to confuse anyone.

Everything that I have read suggests that there is very little genetic contribution to WG. This is not to say that genes are not involved. Clearly, the production of the main antigens in WG, MPO and PR-3, are genetically directed. But what turns their specific genes on and off? No one seems to know. If you know of any papers out of Stanford that can shed more light on this, I would love to know of them.

Al

[me2]

Well, that is an interesting article. Thanks. through which I found another interesting article

Integrating autoimmune risk loci with gene-ex... [Am J Hum Genet. 2011] - PubMed - NCBI (http://www.ncbi.nlm.nih.gov/pubmed/21963258)

[Al]

Well, that is an interesting article. Thanks. through which I found another interesting article

Integrating autoimmune risk loci with gene-ex... [Am J Hum Genet. 2011] - PubMed - NCBI (http://www.ncbi.nlm.nih.gov/pubmed/21963258)
I think this is the way that gene studies will have to go--toward, that is, by statistical analysis. Any specific expressed gene is unlikely to be purely causal. but there are are many statistical correlations that are potentially elucidating.

Al