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Review
. 2022 Mar;35(2):381-395.
doi: 10.1007/s40620-021-01153-4. Epub 2021 Nov 26.

The innate immune system in human kidney inflammaging

Vincenzo Sepe  1 , Carmelo Libetta  2   3 , Marilena Gregorini  2   3 , Teresa Rampino  2
Affiliations
Review

The innate immune system in human kidney inflammaging

Vincenzo Sepe et al. J Nephrol. 2022 Mar.

Abstract

Elderly individuals with chronic disorders tend to develop inflammaging, a condition associated with elevated levels of blood inflammatory markers, and increased susceptibility to chronic disease progression. Native and adaptive immunity are both involved in immune system senescence, kidney fibrosis and aging. The innate immune system is characterized by a limited number of receptors, constantly challenged by self and non-self stimuli. Circulating and kidney resident myeloid and lymphoid cells are all equipped with pattern recognition receptors (PRRs). Recent reports on PRRs show kidney overexpression of toll-like receptors (TLRs) in inflammaging autoimmune renal diseases, vasculitis, acute kidney injury and kidney transplant rejection. TLR upregulation leads to proinflammatory cytokine induction, fibrosis, and chronic kidney disease progression. TLR2 blockade in a murine model of renal ischemia reperfusion injury prevented the escape of natural killer cells and neutrophils by inflammaging kidney injury. Tumor necrosis factor-α blockade in endothelial cells with senescence-associated secretory phenotype significantly reduced interleukin-6 release. These findings should encourage experimental and translational clinical trials aimed at modulating renal inflammaging by native immunity blockade.

Keywords: Acute kidney injury; Aging; COVID-19; Hemodialysis; Inflammaging; Innate immune system.

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Conflict of interest statement

All authors have no conflict of interest to disclose.

Figures

Fig. 1
Fig. 1
PRRs and IL-6 blockade as potential treatment to modulate inflammaging and accelerated renal aging. PRRs pattern recognition receptors, TLRs toll-like receptors, CTLRs C-type lectin receptors, NLRs NOD-like receptors, RLRs RIG-I-like helicase receptors, ROS reactive oxygen species, IL-6 interleukin-6
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