Imperial College London
Alternate

Professor Francis Drobniewski

Faculty of Medicine, Department of Infectious Disease

Chair in Global Health and Tuberculosis
 
 
 
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Contact

 

f.drobniewski

 
 
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Location

 

Commonwealth BuildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Benet:2021:10.1002/jev2.12046,
author = {Benet, S and Galvez, C and Drobniewski, F and Kontsevaya, I and Arias, L and Monguio-Tortajada, M and Erkizia, I and Urrea, V and Ong, R-Y and Luquin, M and Dupont, M and Chojnacki, J and Dalmau, J and Cardona, P and Neyrolles, O and Lugo-Villarino, G and Verollet, C and Julian, E and Furrer, H and Gunthard, HF and Crocker, PR and Tapia, G and Borras, FE and Fellay, J and McLaren, PJ and Telenti, A and Cardona, P-J and Clotet, B and Vilaplana, C and Martinez-Picado, J and Izquierdo-Useros, N},
doi = {10.1002/jev2.12046},
journal = {Journal of Extracellular Vesicles},
pages = {1--17},
title = {Dissemination of Mycobacterium tuberculosis is associated to a SIGLEC1 null variant that limits antigen exchange via trafficking extracellular vesicles},
url = {http://dx.doi.org/10.1002/jev2.12046},
volume = {10},
year = {2021}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - The identification of individuals with null alleles enables studying how the loss of gene function affects infection. We previously described a nonfunctional variant in SIGLEC1, which encodes the myeloidcell receptor Siglec1/CD169 implicated in HIV1 celltocell transmission. Here we report a significant association between the SIGLEC1 null variant and extrapulmonary dissemination of Mycobacterium tuberculosis (Mtb) in two clinical cohorts comprising 6,256 individuals. Local spread of bacteria within the lung is apparent in Mtbinfected Siglec1 knockout mice which, despite having similar bacterial load, developed more extensive lesions compared to wild type mice. We find that Siglec1 is necessary to induce antigen presentation through extracellular vesicle uptake. We postulate that lack of Siglec1 delays the onset of protective immunity against Mtb by limiting antigen exchange via extracellular vesicles, allowing for an early local spread of mycobacteria that increases the risk for extrapulmonary dissemination.
AU  - Benet,S
AU  - Galvez,C
AU  - Drobniewski,F
AU  - Kontsevaya,I
AU  - Arias,L
AU  - Monguio-Tortajada,M
AU  - Erkizia,I
AU  - Urrea,V
AU  - Ong,R-Y
AU  - Luquin,M
AU  - Dupont,M
AU  - Chojnacki,J
AU  - Dalmau,J
AU  - Cardona,P
AU  - Neyrolles,O
AU  - Lugo-Villarino,G
AU  - Verollet,C
AU  - Julian,E
AU  - Furrer,H
AU  - Gunthard,HF
AU  - Crocker,PR
AU  - Tapia,G
AU  - Borras,FE
AU  - Fellay,J
AU  - McLaren,PJ
AU  - Telenti,A
AU  - Cardona,P-J
AU  - Clotet,B
AU  - Vilaplana,C
AU  - Martinez-Picado,J
AU  - Izquierdo-Useros,N
DO  - 10.1002/jev2.12046
EP  - 17
PY  - 2021///
SN  - 2001-3078
SP  - 1
TI  - Dissemination of Mycobacterium tuberculosis is associated to a SIGLEC1 null variant that limits antigen exchange via trafficking extracellular vesicles
T2  - Journal of Extracellular Vesicles
UR  - http://dx.doi.org/10.1002/jev2.12046
UR  - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000614049700009&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR  - https://onlinelibrary.wiley.com/doi/10.1002/jev2.12046
UR  - http://hdl.handle.net/10044/1/86485
VL  - 10
ER  -
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