Emory Report
March 16, 2009
Volume 61, Number 23



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March 16
, 2009
Rheumatoid arthritis cells age chromosomes early

By Quinn Eastman

Telomeres, structures that cap the ends of cells’ chromosomes, grow shorter with each round of cell division unless a specialized enzyme replenishes them. Maintaining telomeres is thought to be important for healthy aging and cancer prevention.

By this measure, T cells, or white blood cells, from patients with the autoimmune disease rheumatoid arthritis are worn out and prematurely aged, scientists at Emory School of Medicine have discovered.

Compared with cells from healthy people, T cells from patients with rheumatoid arthritis have trouble turning on the enzyme that replenishes telomeres, they found.

The results were published online March 2 in Proceedings of the National Academy of Sciences.

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 because of a limited T cell pool, says immunologist Cornelia Weyand.

T cells are some of the very few cells in adults that can turn on the enzyme telomerase when stimulated, probably because they have to divide many times and stay alive for decades. Telomerase is active in embryonic development but is usually switched off in adult cells.

Many cancer cells activate telomerase to enable runaway growth, thus any treatment to reactivate the enzyme would have to be carefully targeted.