But there was no indication that the interaction between the CD86 protein and a T cell had any influence on the B cell itself.
Earlier work by Sanders and her laboratory, however, strongly suggest the CD86 protein did alter the behavior of the B cell. She and her research team showed that B cells produce much more antibody when CD86 interacts with its T-cell protein than occurs when that interaction is missing.
For this study, Sanders and Kin used two groups of laboratory-grown mouse B cells, which are easier to grow than human B cells.
Then they stimulated one group of B cells with all the signals provided by T cells, including the interaction of CD86 and its T-cell protein. The second group of B cells received all the T-cell signals, except the one for CD86.
The researchers then compared the two groups for changes in antibody levels and changes in the signaling molecules associated with antibody production inside the B cells. This enabled the scientists to trace the chemical changes that begin with CD86 and run through the B cell and the making of antibodies.
"We showed for the first time what signaling molecules are activated inside B cells when CD86 is stimulated," says first author Nicholas W. Kin, a graduate research associate in Sanders' laboratory. "We also found that the signals converge on a protein that controls antibody production.
"This is another piece in the complex puzzle of how the immune system works and how it might be manipulated to fight cancer and autoimmune diseases," Kin adds.
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Contact: Darrell E. Ward
Darrell.Ward@osumc.ed
614-293-3737
Ohio State University
2-Aug-2006