Thursday, August 17, 2006
Providence, Rhode Island - When bacteria, viruses or parasites attack, immune system cells unleash the soldiers. These "hot" protein compounds kill invaders - but also trigger inflammation, which, if unchecked, can destroy tissue, induce shock and kill the host. So immune system cells let loose another protein compound to cool down the immune response.
Precisely how this immune system "thermostat" operates is unclear. The leading hypothesis is that these compounds - which act as furnace and air conditioner - battle it out over control of the system's inflammatory response.
But new research, led by George Yap of Brown University, shows that these cytokines don’t operate independently and in opposition. They operate in harmony and are controlled by the same master. In work published in the Journal of Immunology, Yap and his team show that the "cool" anti-inflammatory protein compound known as Interleukin 10 is activated by Interferon-gamma, a class of proteins secreted by a class of white blood cells known as T helper 1 cells. The team then traced secretion of Interferon-gamma indirectly to tyrosine kinase 2, or tyk2, the same protein that signals "hot" inflammatory cytokines Interleukin 12 and Interferon-alpha and Interferon-beta.
The above news release is based on the paper "Tyk2 Negatively Regulates Adaptive Th1 Immunity by Mediating IL-10 Signaling and Promoting IFN-gamma-Dependent IL-10 Reactivation" (Abstract).
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