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Merck

Selective retention of virus-specific tissue-resident T cells in healed skin after recovery from herpes zoster.

Nature communications (2022-11-15)
Kerry J Laing, Werner J D Ouwendijk, Victoria L Campbell, Christopher L McClurkan, Shahin Mortazavi, Michael Elder Waters, Maxwell P Krist, Richard Tu, Nhi Nguyen, Krithi Basu, Congrong Miao, D Scott Schmid, Christine Johnston, Georges M G M Verjans, David M Koelle
RESUMEN

Herpes zoster is a localized skin infection caused by reactivation of latent varicella-zoster virus. Tissue-resident T cells likely control skin infections. Zoster provides a unique opportunity to determine if focal reinfection of human skin boosts local or disseminated antigen-specific tissue-resident T cells. Here, we show virus-specific T cells are retained over one year in serial samples of rash site and contralateral unaffected skin of individuals recovered from zoster. Consistent with zoster resolution, viral DNA is largely undetectable on skin from day 90 and virus-specific B and T cells decline in blood. In skin, there is selective infiltration and long-term persistence of varicella-zoster virus-specific T cells in the rash site relative to the contralateral site. The skin T cell infiltrates express the canonical tissue-resident T cell markers CD69 and CD103. These findings show that zoster promotes spatially-restricted long-term retention of antigen-specific tissue-resident T cells in previously infected skin.

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Anti-Varicella-Zoster Virus Antibody, Glycoprotein I, Chemicon®, from mouse