When small protein fragments or nucleic acids derived from an invading pathogen are detected by pattern recognition receptors on immune cells, the innate immune response is triggered. This event activates cells of the adaptive immune system and, together, both responses clear the infection. Infections also induce the release of “danger-associated molecular patterns,” or alarmins, from the host as a result of tissue damage. Whether these are also important for the ensuing immune response is less clear. Bonilla et al. report that the alarmin interleukin-33 is required for optimal cytotoxic CD8+ T cell responses and antiviral immunity in mice. In virus-infected mice deficient in IL-33 or its receptor, IL-33 is essential for signaling CD8+ T cells to expand, produce multiple cytokines, and acquire cytotoxic capabilities. These results showed that endogenous materials, independently of pathogen-derived molecules, are also required for antiviral immunity.
W. V. Bonilla, A. Fröhlich, K. Senn, S. Kallert, M. Fernandez, S. Johnson, M. Kreutzfeldt, A. N. Hegazy, C. Schrick, P. G. Fallon, R. Klemenz, S. Nakae, H. Adler, D. Merkler, M. Löhning, D. D. Pinschewer, The alarmin interleukin-33 drives protective antiviral CD8+ T cell responses. Science 335, 984–989 (2012). [Abstract] [Full Text]