Imperial College London
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ProfessorJessicaStrid

Faculty of Medicine, Department of Immunology and Inflammation

Professor of Cellular Immunology
 
 
 
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Contact

 

+44 (0)20 3313 1475j.strid

 
 
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Location

 

9N15BCommonwealth BuildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Zhou:2022:10.1126/science.abd5926,
author = {Zhou, L and Kong, G and Palmisano, I and Cencioni, MT and Danzi, M and De, Virgiliis F and Chadwick, JS and Crawford, G and Yu, Z and De, Winter F and Lemmon, V and Bixby, J and Puttagunta, R and Verhaagen, J and Pospori, C and Lo, Celso C and Strid, J and Botto, M and Di, Giovanni S},
doi = {10.1126/science.abd5926},
journal = {Science},
pages = {1--15},
title = {Reversible CD8 T cell-neuron cross-talk causes aging-dependent neuronal regenerative decline.},
url = {http://dx.doi.org/10.1126/science.abd5926},
volume = {376},
year = {2022}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - INTRODUCTIONAxonal regeneration and neurological functional recovery are extremely limited in the elderly. Consequently, injuries to the nervous system are typically followed by severe and long-term disability. Our understanding of the molecular mechanisms underlying aging-dependent regenerative failure is poor, hindering progress in the development of effective therapies for neurological repair. To facilitate the design of repair strategies, there is a pressing need to identify critical molecular and cellular mechanisms that cause regenerative failure in aging.RATIONALEAging causes a broad spectrum of modifications in cell signaling, including changes in metabolism, immunity, and overall tissue homeostasis, which play key roles in nervous system physiology and response to insults. Thus, we hypothesized that injuries to the aged nervous system would be followed by unique molecular and cellular modifications that would contribute to aging-dependent regenerative decline. To this end, molecular and cellular signatures associated with aging and injury to the nervous system were systematically investigated by performing RNA sequencing from dorsal root ganglia (DRG) in a well-established model of sciatic nerve injury in young versus aged mice. Insight into these mechanisms could allow the discovery of previously unrecognized molecular targets to counteract aging-dependent regenerative decline.RESULTSInitial analysis of RNA sequencing data identified that aging was mainly associated with a marked increase in T cell activation and signaling in DRG after sciatic nerve injury in mice. Subsequent experiments demonstrated that aging was associated with increased inflammatory cytokines including lymphotoxins in DRG both preceding and following sciatic nerve injury. Specifically, we found that lymphotoxin β was required for the phosphorylation of NF-κB that drives the expression of the chemokine CXCL13 in DRG sensory neurons. CXCL13 attracted CD8+ T cells that expresse
AU  - Zhou,L
AU  - Kong,G
AU  - Palmisano,I
AU  - Cencioni,MT
AU  - Danzi,M
AU  - De,Virgiliis F
AU  - Chadwick,JS
AU  - Crawford,G
AU  - Yu,Z
AU  - De,Winter F
AU  - Lemmon,V
AU  - Bixby,J
AU  - Puttagunta,R
AU  - Verhaagen,J
AU  - Pospori,C
AU  - Lo,Celso C
AU  - Strid,J
AU  - Botto,M
AU  - Di,Giovanni S
DO  - 10.1126/science.abd5926
EP  - 15
PY  - 2022///
SN  - 0036-8075
SP  - 1
TI  - Reversible CD8 T cell-neuron cross-talk causes aging-dependent neuronal regenerative decline.
T2  - Science
UR  - http://dx.doi.org/10.1126/science.abd5926
UR  - https://www.ncbi.nlm.nih.gov/pubmed/35549409
UR  - https://www.science.org/doi/10.1126/science.abd5926
VL  - 376
ER  -
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