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Pulling T cells to pathogens

Nature Biotechnology volume 30, page 1206 (2012)Cite this article

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After entering the vaginal cavity, HSV-2— the causative agent of genital herpes— replicates in mucosal epithelial cells before spreading to innervating neurons and establishing latency within the dorsal root ganglia. HSV-2 periodically reawakens from dormancy and infects and kills mucosal epithelial cells. These reactivations cause the characteristic lesions of clinical genital herpes.

The strategy developed by Shin and Iwasaki1 exploits the normal defensive process triggered by HSV-2 infection whereby T cells are attracted to infected mucosa in response to virus-induced inflammation. In mice, HSV-2 infection causes CD4+ T- cell production of interferon-γ, which elicits production of the chemokines CXCL9 and CXCL10, which in turn recruit effector CD8+ T cells expressing CXCR3, the receptor for CXCL9 and CXCL10. The authors reasoned that mimicking just one step of this inflammatory cascade—production of CXCL9 and CXCL10—might pull in protective T cells while bypassing unwanted vaginal inflammation.

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References

  1. Shin, H. & Iwasaki, A. Nature advance online publication, 10.1038/nature11522 (2012).

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  1. Senior Editor, Nature Biotechnology,

    Christine Borowski

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  1. Christine Borowski
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Borowski, C. Pulling T cells to pathogens. Nat Biotechnol 30, 1206 (2012). https://doi.org/10.1038/nbt.2445

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