Accelarated immune ageing is associated with COVID-19 disease severity.
Journal
Immunity & ageing : I & A
ISSN: 1742-4933
Titre abrégé: Immun Ageing
Pays: England
ID NLM: 101235427
Informations de publication
Date de publication:
11 Jan 2024
11 Jan 2024
Historique:
received:
04
07
2023
accepted:
18
12
2023
medline:
12
1
2024
pubmed:
12
1
2024
entrez:
11
1
2024
Statut:
epublish
Résumé
The striking increase in COVID-19 severity in older adults provides a clear example of immunesenescence, the age-related remodelling of the immune system. To better characterise the association between convalescent immunesenescence and acute disease severity, we determined the immune phenotype of COVID-19 survivors and non-infected controls. We performed detailed immune phenotyping of peripheral blood mononuclear cells isolated from 103 COVID-19 survivors 3-5 months post recovery who were classified as having had severe (n = 56; age 53.12 ± 11.30 years), moderate (n = 32; age 52.28 ± 11.43 years) or mild (n = 15; age 49.67 ± 7.30 years) disease and compared with age and sex-matched healthy adults (n = 59; age 50.49 ± 10.68 years). We assessed a broad range of immune cell phenotypes to generate a composite score, IMM-AGE, to determine the degree of immune senescence. We found increased immunesenescence features in severe COVID-19 survivors compared to controls including: a reduced frequency and number of naïve CD4 and CD8 T cells (p < 0.0001); increased frequency of EMRA CD4 (p < 0.003) and CD8 T cells (p < 0.001); a higher frequency (p < 0.0001) and absolute numbers (p < 0.001) of CD28 Our analyses reveal a state of enhanced immune ageing in survivors of severe COVID-19 and suggest this could be related to SARS-Cov-2 infection. Our data support the rationale for trials of anti-immune ageing interventions for improving clinical outcomes in these patients with severe disease.
Sections du résumé
BACKGROUND
BACKGROUND
The striking increase in COVID-19 severity in older adults provides a clear example of immunesenescence, the age-related remodelling of the immune system. To better characterise the association between convalescent immunesenescence and acute disease severity, we determined the immune phenotype of COVID-19 survivors and non-infected controls.
RESULTS
RESULTS
We performed detailed immune phenotyping of peripheral blood mononuclear cells isolated from 103 COVID-19 survivors 3-5 months post recovery who were classified as having had severe (n = 56; age 53.12 ± 11.30 years), moderate (n = 32; age 52.28 ± 11.43 years) or mild (n = 15; age 49.67 ± 7.30 years) disease and compared with age and sex-matched healthy adults (n = 59; age 50.49 ± 10.68 years). We assessed a broad range of immune cell phenotypes to generate a composite score, IMM-AGE, to determine the degree of immune senescence. We found increased immunesenescence features in severe COVID-19 survivors compared to controls including: a reduced frequency and number of naïve CD4 and CD8 T cells (p < 0.0001); increased frequency of EMRA CD4 (p < 0.003) and CD8 T cells (p < 0.001); a higher frequency (p < 0.0001) and absolute numbers (p < 0.001) of CD28
CONCLUSIONS
CONCLUSIONS
Our analyses reveal a state of enhanced immune ageing in survivors of severe COVID-19 and suggest this could be related to SARS-Cov-2 infection. Our data support the rationale for trials of anti-immune ageing interventions for improving clinical outcomes in these patients with severe disease.
Identifiants
pubmed: 38212801
doi: 10.1186/s12979-023-00406-z
pii: 10.1186/s12979-023-00406-z
pmc: PMC10782727
doi:
Types de publication
Journal Article
Langues
eng
Pagination
6Subventions
Organisme : Medical Research Council
ID : MC_PC_20031
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_PC_20060
Pays : United Kingdom
Organisme : British Heart Foundation
ID : CH/16/2/32089
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/V040162/1
Pays : United Kingdom
Organisme : British Heart Foundation
ID : CH/F/21/90010
Pays : United Kingdom
Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : British Heart Foundation
ID : RG/16/1/32092
Pays : United Kingdom
Investigateurs
K Abel
(K)
H Adamali
(H)
D Adeloye
(D)
O Adeyemi
(O)
R Adrego
(R)
L A AguilarJimenez
(LA)
S Ahmad
(S)
N Ahmad Haider
(N)
R Ahmed
(R)
N Ahwireng
(N)
M Ainsworth
(M)
B Al-Sheklly
(B)
A Alamoudi
(A)
M Ali
(M)
M Aljaroof
(M)
A M All
(AM)
L Allan
(L)
R J Allen
(RJ)
L Allerton
(L)
L Allsop
(L)
P Almeida
(P)
D Altmann
(D)
M Alvarez Corral
(M)
S Amoils
(S)
D Anderson
(D)
C Antoniades
(C)
G Arbane
(G)
A Arias
(A)
C Armour
(C)
L Armstrong
(L)
N Armstrong
(N)
D Arnold
(D)
H Arnold
(H)
A Ashish
(A)
A Ashworth
(A)
M Ashworth
(M)
S Aslani
(S)
H Assefa-Kebede
(H)
C Atkin
(C)
P Atkin
(P)
R Aul
(R)
H Aung
(H)
L Austin
(L)
C Avram
(C)
A Ayoub
(A)
M Babores
(M)
R Baggott
(R)
J Bagshaw
(J)
D Baguley
(D)
L Bailey
(L)
J K Baillie
(JK)
S Bain
(S)
M Bakali
(M)
M Bakau
(M)
E Baldry
(E)
D Baldwin
(D)
M Baldwin
(M)
C Ballard
(C)
A Banerjee
(A)
B Bang
(B)
R E Barker
(RE)
L Barman
(L)
S Barratt
(S)
F Barrett
(F)
D Basire
(D)
N Basu
(N)
M Bates
(M)
A Bates
(A)
R Batterham
(R)
H Baxendale
(H)
H Bayes
(H)
M Beadsworth
(M)
P Beckett
(P)
M Beggs
(M)
M Begum
(M)
P Beirne
(P)
D Bell
(D)
R Bell
(R)
K Bennett
(K)
E Beranova
(E)
A Bermperi
(A)
A Berridge
(A)
C Berry
(C)
S Betts
(S)
E Bevan
(E)
K Bhui
(K)
M Bingham
(M)
K Birchall
(K)
L Bishop
(L)
K Bisnauthsing
(K)
J Blaikely
(J)
A Bloss
(A)
A Bolger
(A)
C E Bolton
(CE)
J Bonnington
(J)
A Botkai
(A)
C Bourne
(C)
M Bourne
(M)
K Bramham
(K)
L Brear
(L)
G Breen
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J Breeze
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A Briggs
(A)
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(E)
S Brill
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K Brindle
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A Broadley
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J Brown
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J Brown
(J)
J S Brown
(JS)
M Brown
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V Brown
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T Brugha
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N Brunskill
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M Buch
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P Buckley
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A Bularga
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R Butcher
(R)
A Butt
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P Cairns
(P)
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B Card
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A Charalambou
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N Chaudhuri
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A Checkley
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J Chen
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Y Cheng
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E R Chilvers
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P Chowienczyk
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C Favager
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J Featherstone
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J Finnigan
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L Finnigan
(L)
H Fisher
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R Flockton
(R)
M Flynn
(M)
H Foot
(H)
D Foote
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A Ford
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D Forton
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E Fraile
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C Francis
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A Frankel
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N French
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P L Greenhaff
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W Greenhalf
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H Gregory
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D Grieve
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I Hall
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A Hancock
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N A Hanley
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(HE)
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(E)
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B Hargadon
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(E)
V C Harris
(VC)
E M Harrison
(EM)
P Harrison
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N Hart
(N)
A Harvey
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L G Heaney
(LG)
C Heeley
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(JL)
M Heightman
(M)
S Heller
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M Henderson
(M)
L Hesselden
(L)
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(M)
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(LP)
A Hoare
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(P)
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(S)
L Holdsworth
(L)
D Holgate
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M Holland
(M)
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(L)
K Holmes
(K)
M Holmes
(M)
B Holroyd-Hind
(B)
L Holt
(L)
A Hormis
(A)
A Horsley
(A)
A Hosseini
(A)
M Hotopf
(M)
L Houchen-Wolloff
(L)
K Howard
(K)
L S Howard
(LS)
A Howell
(A)
E Hufton
(E)
A D Hughes
(AD)
J Hughes
(J)
R Hughes
(R)
A Humphries
(A)
N Huneke
(N)
E Hurditch
(E)
J Hurst
(J)
M Husain
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T Hussell
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J Hutchinson
(J)
W Ibrahim
(W)
F Ilyas
(F)
J Ingham
(J)
L Ingram
(L)
D Ionita
(D)
K Isaacs
(K)
K Ismail
(K)
T Jackson
(T)
J Jacob
(J)
W Y James
(WY)
W Jang
(W)
C Jarman
(C)
I Jarrold
(I)
H Jarvis
(H)
R Jastrub
(R)
B Jayaraman
(B)
R G Jenkins
(RG)
P Jezzard
(P)
K Jiwa
(K)
C Johnson
(C)
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(S)
D Johnston
(D)
C J Jolley
(CJ)
D Jones
(D)
G Jones
(G)
H Jones
(H)
H Jones
(H)
I Jones
(I)
L Jones
(L)
M G Jones
(MG)
S Jones
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Informations de copyright
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