http://med.stanford.edu/news/all-ne...N8vVv12VaG7ZzgU-JbX6aXhQ76Q7Nl2aNngURzGngCfqM
The errant cells are helper T cells. After infiltrating synovial tissue, they send out signals that call in other super-aggressive immune cells and cause ordinary synovial cells to become inflamed and destructive.
In prior work, Weyand’s group noticed telling differences between the helper T cells of patients with rheumatoid arthritis and those of healthy people. The former, for instance, have low reserves of a molecule called ATP, which serves as cells' internal energy currency, accepted by all of a cell’s myriad metabolic enterprises. Yet instead of directing their primary energy source, glucose, toward ATP production, these cells divert their glucose supplies toward fashioning various materials — proteins, nucleic acids, membranes and the like — used to build new T cells that will contribute to further damage.
That shouldn’t happen. Like all cells, T cells contain AMPK, a regulatory molecule that senses ratios of ATP and its two main breakdown products. If it finds ATP too outnumbered by these breakdown products, AMPK clamps down on the T cell’s cell-building program and, instead, sends glucose off to the cell’s ATP-generating apparatus.
“When your house is cold, you need to throw your logs into your fireplace, not use them to build a new house in your backyard,” Weyand said.
The new study provides an answer to the question of why AMPK fails to perform its energy-monitoring function in the faulty helper T cells of patients with rheumatoid arthritis.
The errant cells are helper T cells. After infiltrating synovial tissue, they send out signals that call in other super-aggressive immune cells and cause ordinary synovial cells to become inflamed and destructive.
In prior work, Weyand’s group noticed telling differences between the helper T cells of patients with rheumatoid arthritis and those of healthy people. The former, for instance, have low reserves of a molecule called ATP, which serves as cells' internal energy currency, accepted by all of a cell’s myriad metabolic enterprises. Yet instead of directing their primary energy source, glucose, toward ATP production, these cells divert their glucose supplies toward fashioning various materials — proteins, nucleic acids, membranes and the like — used to build new T cells that will contribute to further damage.
That shouldn’t happen. Like all cells, T cells contain AMPK, a regulatory molecule that senses ratios of ATP and its two main breakdown products. If it finds ATP too outnumbered by these breakdown products, AMPK clamps down on the T cell’s cell-building program and, instead, sends glucose off to the cell’s ATP-generating apparatus.
“When your house is cold, you need to throw your logs into your fireplace, not use them to build a new house in your backyard,” Weyand said.
The new study provides an answer to the question of why AMPK fails to perform its energy-monitoring function in the faulty helper T cells of patients with rheumatoid arthritis.