Natural immune-control system may aid treatment of autoimmune disease and tissue rejection

y to spark an immune attack.

Antibody-based treatments fall short for a variety of reasons: the antibodies often fail to fit securely inside T cells receptors, so the immune response is only slightly reduced; or the antibodies succeed in blocking the receptor, but that inadvertently causes the T cells to launch a more ferocious attack. In other cases, antibodies work too well, suppressing the entire immune system, rather than just a portion of it, leaving patients susceptible to dangerous infections.

To overcome these problems, researchers have tried to harness the body's natural system for quieting the immune response. One intriguing approach involves the immune system's "natural killer," or NK, cells. Scientists have long known that some NK cells can kill a class of T cells -- known as CD4 T cells -- that have been activated to fight infection, but that NK cells are often restrained from doing so.

Cantor and his colleagues theorized that when a tiny hook, or ligand, called Qa-1Qdm on activated CD4 T cells latches onto the NKG2A receptor on NK cells, the T cells are protected from destruction. To test this, they produced activated T cells that either lacked the Qa-1Qdm receptor or had a faulty version of it, preventing them from binding to the NKG2A receptor. The result was that the T cells became vulnerable to attack from a set of NK cells. Using an antibody to block the connection between Qa-1Qdm and NKG2A had the same result.

"Our findings suggest that it is possible to use antibodies to trigger the body's own mechanism for suppressing the immune response," Cantor remarks. "The results serve as a proof of principle that this approach can be applied to the treatment of conditions characterized by an excessive or unwanted immune response."

While the work was done with mouse cells, the Qa-1Qdm ligand has the same shape and structure in human and mouse T cells, raising hopes that the approach will prove effective in

Contact: Bill Schaller
Dana-Farber Cancer Institute

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