Can Germs Prevent Arthritis?
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T-cells and the Innate Immune System
Exactly how infection might trigger RA or other diseases is not yet clear, but a better understanding of the immune system and the cleanliness theory offers some clues.
Scientists have known that people have two overlapping immune systems – the adaptive immune system, which takes time to develop, and the innate immune system, which people have at birth. The adaptive immune system is the one that enables your body to form antibodies to specific infectious invaders that sneak in and threaten your health.
But your body can’t wait until it has formed those specific antibodies – a process that takes about a week – to start fighting infections. That’s where the innate immune system comes in.
“If you get pneumonia, your body has to react fast. Its innate immune system goes into action, calling forth a lot of different responses in rapid progression,” Dr. Sarvetnick says. “The innate system is more primitive – it is the broader sweeping and more rapidly responding immune system.”
That sweep, in some cases, may be a bit too broad. While helping the body react and respond quickly to an invading organism it may react too vigorously, triggering an autoimmune response against the body’s healthy tissues in someone genetically predisposed.
If an infectious organism can trigger an autoimmune disease, how could avoiding infections be harmful? When our bodies are exposed to infectious organisms, scavenger cells called macrophages – are stimulated to fight the invader and call in white blood cells such as T cells. That stimulation strengthens the immune system. When such infections are absent, however, the T cells don’t receive the necessary stimulation and begin to die off, says Sarvetnick, which weakens the immune system.
When the body senses that T-cell levels are low, it tries to correct the deficiency by inducing the remaining T cells to multiply quickly. Unfortunately, rapid growth and turnover promotes the formation of an abundance of aggressive, autoreactive T cells that turn against the body and cause autoimmune disease, says Sarvetnick.
Sarvetnick says better understanding the T-cell depletion that results from lack of exposure to infections may lead to new therapies. Her group has found a protein called interleukin-21 (IL-21), which makes T cells divide. Eventually agents that block IL-21 or work in other ways to stop T-cell multiplication could be investigated as therapies to keep the aggressive autoreactive T cells from causing autoimmunity.
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