Tim-3 Proteins Shut Down Immune Attack

Researchers have found that the Tim-3 surface protein found on TH1-type helper T cells plays a key role in regulating immune response through modulation of helper cell activity in order to prevent tissue inflammation and development of autoimmune diseases.

Investigators at Harvard Medical School (Boston, MA, USA) used a line of mice with autoimmune diabetes, a condition known to be caused by a TH1 response against insulin-producing cells, to show that the Tim-3 pathway blockade accelerated diabetes in nonobese diabetic mice and prevented acquisition of transplantation tolerance induced by co-stimulation blockade. These findings were published in two papers in the November 2003 issue of Nature Immunology.

"Activated TH1-type helper T cells both participate in and help orchestrate the attack on cells bearing proteins, thereby guarding against infection,” explained senior author Terry Strom, M.D., professor of medicine at Harvard Medical School. "The particular pattern of Tim-3 expression that was found in these two studies suggests that it plays a key role in squelching activation of TH1 T-cells. Nature must have wanted us to have such a mechanism so that once you have created immunity, you have a timely means of ‘turning off' the immune attack.”




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