Washington, Mar 5 (ANI): Scientists at Emory University School of Medicine have discovered that T cells, or white blood cells, from patients with the autoimmune disease rheumatoid arthritis have prematurely aged chromosomes due to lack of structures called telomeres.
elomeres are structures that cap the ends of cells' chromosomes, grow shorter with each round of cell division unless a specialized enzyme replenishes them.
It is important to maintain telomeres as they are thought to be important for healthy aging and cancer prevention.
T cells from patients with rheumatoid arthritis were found to have trouble turning on the enzyme that replenishes telomeres, when compared with cells from healthy people.
Reversing this defect could possibly help people prone to the disease maintain a balanced immune system.
Senior author Cornelia Weyand, MD, PhD said that in rheumatoid arthritis, T cells are chronically over-stimulated, invading the tissue of the joints and causing painful inflammation.
She claimed that in childhood, new T cells are continually produced in the thymus, but after about age 40, the thymus "involutes" - or shrinks and ceases to function. After that, the immune system has to make do with the pool of T cells it already has.
"What we see in rheumatoid arthritis is an aged and more restricted T cell repertoire. This biases the immune system toward autoimmunity," she said.
Intrigued by earlier studies claiming that in rheumatoid arthritis, T cells tend to shift the molecules on their surface and function differently, the researchers wanted to study the mechanisms of T cells' premature aging.
They found the answer in telomerase, the enzyme that renews telomeres and is necessary to prevent loss of genetic information after repeated cell division.
Telomerase adds short repeated DNA sequences to the ends of chromosomes to protect them. The enzyme is active in embryonic development but is usually switched off in adult cells. Many cancer cells reactivate it to enable runaway growth.
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.
Researchers found that T cells from patients with rheumatoid arthritis make 40 percent less telomerase enzyme when stimulated.
The cells came from 69 patients, 92 percent female, with an average age of 50, and were compared with cells from healthy people with similar demographics.
By shutting off a gene encoding part of the enzyme normal T cells were made vulnerable to programmed cell death, and transferring telomerase into patients' T cells rescued them from dying.
Scientists said that the finding suggests that restoring defective telomerase to T cells could possibly help "reset" the immune system in rheumatoid arthritis.
The results are published online in Proceedings of the National Academy of Sciences. (ANI)