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Targeting immune cell-neuron crosstalk restores youthfulness to aging neurons

 Last Update: 2022-08-11
 Source: Internet
 Author: User

T cells in older adults touch nerves

As we age, the ability to recover from neurological damage becomes increasingly limit.

However, the molecular and cellular mechanisms of aging-dependent regenerative decline remain uncle.

As a result, damage to the nervous system is often accompanied by severe and long-term disabili.

Therefore, we hypothesized that damage to the aged nervous system is followed by unique molecular and cellular modifications leading to a decline in age-dependent regenerati.

Subsequent experiments showed that aging was associated with increased inflammatory cytokines, including lymphotoxin, in the DRG before and after sciatic nerve inju.

⁺CD8⁺T cells close to sensory neurons, after communicating with MHC I, limit axonal regeneration after nerve injury, presenting DRG neuro.

Sequence of events leading to failure of aging-dependent regeneration of damaged sensory neuro.

(1) Lymphotoxin beta activates NF-κB;

(2) Phosphorylation of NF-κB increases the expression of CXCL13;(3) CXCR5 type⁺CD8⁺T cells enter the DRG parenchyma;(4,5) Sciatic axonal injury activates the injury signal;(6) MHC I is presented by DRG neurons;(7) CXCR5 type⁺CD8⁺T cells bind to MHC I and activate neuronal caspase3;(8) Cleaved caspase3 reduces pAKT and pS6, resulting in regeneration failu.

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