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IL-33, released from necrotic cells, mobilizes killer T cells to respond to viral infections.

Tissue trauma is recognized by receptor-mediated detection of certain alarmins, proteins released from dead cells. However, the contribution of alarmins to antiviral immune defense has remained poorly defined. A team headed by Professors Daniel Pinchewer (University of Geneva) and Max Löhning (Charité-University of Medicine & DRFZ Berlin) discovered that viral replication causes the death of infected cells in the spleen and lymph nodes. These necrotic cells release interleukin-33 (IL-33) which notifies CD8+ T cells (CTLs) of the infection (Bonilla (2012) Science. PMID: 22323740). IL-33 is the principal alarmin discharged from the dying cells, and is necessary for the potent CTL response to replicating viruses. IL-33 signals through the ST2 receptor on activated CTLs, to promote virus control. Mice deficient in IL-33 displayed a reduced CTL response to viral infections. The findings highlight a new mechanism whereby nonhematopoietic cells release alarmins to mobilize CTL response to infection. This could be exploited to create vaccines against infectious diseases such as HIV and hepatitis C, as well as in the treatment of cancer.

Enzo Life Sciences offers a wide range of products relating to necrosis, as well as innate and adaptive immunity. Many of these products are relevant to the investigation of IL-33 as an alarmin.

 

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