Telomeres and Autoimmune Disease

An interesting correlation to add to the others involving telomerase:

In rheumatoid arthritis, T cells are chronically over-stimulated, invading the tissue of the joints and causing painful inflammation. This derangement can be seen as a result of the loss of the immune system's ability to discriminate friend from foe


"What we see in rheumatoid arthritis is an aged and more restricted T cell repertoire," she says. "This biases the immune system toward autoimmunity."


They found the answer in telomerase, the enzyme that renews telomeres and is necessary to prevent loss of genetic information after repeated cell division.


T cells are some of the very few cells in adults that can turn on telomerase when stimulated, probably because they have to divide many times and stay alive for decades. Weyand and Fujii found that T cells from patients with rheumatoid arthritis make 40 percent less telomerase enzyme when stimulated.

The researchers suggest that restoring telomerase to T cells could possibly help reset the immune system and halt rheumatoid arthritis, but I think that remains as a conjecture to be proven. Is there a slippery slope of declining telomerase for some people, ending up with immune systems that fall into disfunction at earlier ages? Or does some other aspect of this particular autoimmune disease cause the drop in telomerase production? Identifying the cart and the horse here isn't straightforward.

Telomerase is tied in to more than just telomeres: it seems to influence mitochondrial function as well. Variations in telomerase activity and telomere length are clearly associated with aging and specific age-related conditions, but it's far from clear how it all links together, and all of the interesting new research results I'm aware of from the past couple of years have served to complicate the picture.


There is a growing view that autoimmune disorders, along with the hormonal, enzymatic and other problems that accompany them, are caused by the human microbiota--in other words, that they are pathogen based. This paper, recently accepted by the journal Autoimmunity Reviews, may be of interest:

Proal AD, Albert PJ, Marshall TG. Autoimmunity in the Era of the Metagenome.

A full text preprint is available free of charge from the Foundation:

Posted by: shegeek at March 5th, 2009 3:07 AM

So how do we reconcile this with WILT?

Any ideas?

Posted by: Stuart Calimport at March 6th, 2009 9:53 AM

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