Researchers at the University of Basel have uncovered the key to the tenacity of CD8+ T cells in fighting chronic viral infection. According to the team, their findings, published in Immunity last month, lay the foundation for more effective therapies and vaccination strategies.
“These T cells can become specialized in two different ways: either as a kind of sprinter or as marathon runners,” explains Professor Daniel Pinschewer, senior author of the study. “However, the latter can also convert into sprinters at any time, in order to stamp out an infection.”
Chronic infections are a special case: CD8+are activated and a strong inflammatory response occurs at the same time. “This tends to ‘shock’ the T cells into developing into sprinters, which can only intervene effectively in the short term to remove infected cells,” says Pinschewer. “If all T cells behaved like that, our immune defenses would break down pretty soon.”
In the study, the researchers examined how, in spite of this, the immune system is still able to provide enough CD8+ for the endurance race against chronic infections. According to their results, interleukin-33 (IL-33) plays a key role. It allows the T cells to remain in their “marathon runner” state. “IL-33 takes away the shock of the inflammation, so to speak,” explains Anna-Friederike Marx, lead author of the study.
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In addition, the biological messenger causes the marathon CD8+ to proliferate, so that more endurance runners are available to combat the infection. “Thanks to IL-33, there are enough cytotoxic T cells around for the long haul that can still pull off a final sprint after their marathon,” adds Marx.
The findings could help improve the treatment of chronic infections such as hepatitis C. It is conceivable that IL-33 could be administered to support an effective immune response. Thinking along the same lines, IL-33 could be one key to improving cancer immunotherapy, to enable T cells to wage an efficient and long-lasting offensive against tumor cells.