Paracrine Pass-Through

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Science  28 Aug 2009:
Vol. 325, Issue 5944, pp. 1049
DOI: 10.1126/science.325_1049c

Upon encounter with infectious agents such as viruses, host organisms must rapidly mount a strong system-wide immune response, lest the infection spread dangerously wide. How do they accomplish this task at the early stage when so few cells are typically infected? Patel et al. demonstrate that one mechanism may rely on intercellular communication through gap junctions. They showed that when cells were exposed to double-stranded DNA (dsDNA), which can be found during infection by some types of viruses, not only the cell that directly sensed the dsDNA, but also the surrounding cells, were able to produce pro-inflammatory and antiviral cytokines that are required to initiate the full antiviral immune response. If the gap junctions were blocked through chemical inhibition or by genetic interference, the surrounding cells no longer produced cytokines when their neighbors were exposed to dsDNA. Thus, gap junctions allow the rapid mobilization and amplification of an antiviral immune response by transmitting the activating signal directly from infected cells to uninfected cells.

Proc. Natl. Acad. Sci. U.S.A. 106, 12867 (2009).

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