As most will know, senescent cells lead to a plethora of ageing-related pathophysiologies. In this recent study, Chambers et al. describe how cutaneous senescent fibroblasts are responsible for the non-specific immune response to injection of varicella zoster virus (VZV) antigen. They show that, after needle damage, there is an increase in senescent fibroblasts expressing CCL12, leading to inflammatory monocyte infiltration. These monocytes secrete PGE2, resulting in reduced resident memory T-cell activation and, therefore, a dampened VZV antigen specific response. Using a p38 kinase inhibitor, the authors were able to restore the specific immune response due to decreased CCL12 production in senescent fibroblasts, monocyte recruitment and PGE2 secretion.
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