Researchers have found that Poly-ICLC exacerbates lung damage and bacterial load in mice infected with Mycobacterium tuberculosis, the bacterium that causes tuberculosis. The study published in The Journal of Clinical Investigation suggests that such agents should be used with caution in individuals with dormant M. tuberculosis.
In the study, the marked increase in lung bacterial load and widespread lung damage observed in Poly-ICLC treated M. tuberculosis-infected mice, which was absent in mice lacking the receptor for type I IFNs, was accompanied by a dramatic increase in the number of myeloid immune cells characterized as CD11b+F4/80+Gr1int in the lungs. These cells, which were recruited to the lungs by the chemoattractant CCL2 induced by Poly-ICLC, preferentially supported bacterial growth, providing a mechanistic explanation as to why Poly-ICLC exacerbates lung damage and bacterial load in M. tuberculosis-infected mice.
Type I IFNs, immune molecules that play a central role in antiviral host defense, have been shown to be of clinical benefit in the treatment of a number of viral infections and cancers. Molecules such as Poly-ICLC that potently induce long-lived type I IFN responses have been in clinical trials.
