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Scripps research scientists identify new regulatory mechanism for critical protein signaling domain

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Sauer offers a helpful analogy for the newly uncovered mechanism: "IP4 acts very like a clever engineer. If you were trying to dock your ship at a space station but found that the docking stations weren't fully compatible, the station would send over an engineer called IP4 and he would reconfigure your dock to fit the space station."

Repercussions for T Cell Development

Signaling from T cell receptors triggers the generation of PIP3 and IP4, Sauer explained, leading to the recruitment of proteins to the cell membrane from the cytosol, the internal part of the cell. This receptor signal is part of the mechanisms by which T cells, key players of the immune system, protect us against attack by pathogens such as viruses. However, defective T cell development can lead to a number of immune diseases including allergies like asthma and autoimmune diseases like rheumatoid arthritis, while severely reduced T cell development or function can lead to immunodeficiency diseases such as AIDS.

Using a mouse mutant lacking ItpkB, the enzyme that produces IP4, Sauer and his colleagues showed that without the enzyme, T cells could not develop to maturity.

Because T cell development is regulated by receptor signaling, Sauer said, if the T cell doesn't signal properly, it is normally killed through programmed cell death or other mechanisms. In immature T cells-called double positive cells-if the signal is correct, the cells undergo positive selection in the thymus and are allowed to develop into mature CD4 or CD8 single positive (SP) T cells. Damaged or nonfunctional cells are eliminated.

"IP4 is generated after T cell receptor stimulation," he said. "We found that if IP4 cannot be made due to lack of ItpkB, important signaling molecules including the protein tyrosine kinase Itk can not be properly recruited to the cell membrane. Itk is a key activator of another enzyme, PLC g1, in T- cells. PLC g1 is important for signa
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Contact: Keith McKeown
kmckeown@scripps.edu
858-784-8134
Scripps Research Institute
5-Apr-2007


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