These cells make 40% less telomerase, according to PNAS paper.

T cells from patients with rheumatoid arthritis are worn out and prematurely aged, because their telomeres are not replenished, according to scientists at Emory University School of Medicine.

They say that the T cells have a hard time turning on enzyme telomerase, which rejuvenates telomeres and helps prevent the loss of genetic information.

“What we see in rheumatoid arthritis is an aged and more restricted T-cell repertoire,” says Cornelia Weyand, M.D., Ph.D., senior author of the study. “This biases the immune system toward autoimmunity.”

The researchers found that T cells from patients with rheumatoid arthritis make 40% less telomerase enzyme when stimulated. The cells came from 69 patients, 92% of them female. The average age of the patients was 50, and they were compared with cells from healthy people with similar demographics.

When investigators shut off a gene encoding part of the enzyme, it made normal T cells vulnerable to programmed cell death. Transferring telomerase into patients’ T cells, on the other hand, kept them from dying.

The investigators thus suggest that restoring defective telomerase to T cells could reset the immune system in rheumatoid arthritis.

The results are published online this week in Proceedings of the National Academy of Sciences.

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