During viral infections, activation of the immune pathways that lead to production of interferon - a major mediator of the antiviral response - inhibits production of interleukin 12 (IL-12), a cytokine important for fighting bacterial infections, according to a report published in Nature Immunology.
Various classes of receptors activate immune mediators specifically tailored for the invading pathogen. The signaling pathways activated by these receptors are known to interact in a variety of ways, including cooperation, complementation and compensation. Tadatsugu Taniguchi and colleagues show that IRF3, a transcription factor induced during an antiviral response and essential for production of interferon, directly suppresses transcription of the gene encoding IL-12. Consistent with this observation, the authors note that virus infection attenuated the anti-bacterial response leading to increased mortality in mice at normally sublethal doses of bacteria. This inhibitory interaction might have the advantage of protecting the host from excessive inflammation during an antiviral response, but can have negative implications in co-infections with multiple pathogens.
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