Imperial College London
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DrSophieRutschmann

Faculty of Medicine, Department of Immunology and Inflammation

Reader in Immunology
 
 
 
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Contact

 

s.rutschmann Website

 
 
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Location

 

9N4bHammersmith HospitalHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Ling:2018:10.1126/science.aao4555,
author = {Ling, GS and Crawford, G and Buang, N and Bartok, I and Tian, K and Thielens, NM and Bally, I and Harker, JA and Ashton-Rickardt, PG and Rutschmann, S and Strid, J and Botto, M},
doi = {10.1126/science.aao4555},
journal = {Science},
pages = {558--563},
title = {C1q restrains autoimmunity and viral infection by regulating CD8+ T cell metabolism},
url = {http://dx.doi.org/10.1126/science.aao4555},
volume = {360},
year = {2018}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Deficiency of C1q, the initiator of the complement classical pathway, is associated with the development of systemic lupus erythematosus (SLE). Explaining this association in terms of abnormalities in the classical pathway alone remains problematic because C3 deficiency does not predispose to SLE. Here, using a mouse model of SLE, we demonstrate that C1q, but not C3, restrains the response to self-antigens by modulating the mitochondrial metabolism of CD8+ T cells, which can themselves propagate autoimmunity. C1q deficiency also triggers an exuberant effector CD8+ T cell response to chronic viral infection leading to lethal immunopathology. These data establish a link between C1q and CD8+ T cell metabolism and may explain how C1q protects against lupus, with implications for the role of viral infections in the perpetuation of autoimmunity.
AU  - Ling,GS
AU  - Crawford,G
AU  - Buang,N
AU  - Bartok,I
AU  - Tian,K
AU  - Thielens,NM
AU  - Bally,I
AU  - Harker,JA
AU  - Ashton-Rickardt,PG
AU  - Rutschmann,S
AU  - Strid,J
AU  - Botto,M
DO  - 10.1126/science.aao4555
EP  - 563
PY  - 2018///
SN  - 0036-8075
SP  - 558
TI  - C1q restrains autoimmunity and viral infection by regulating CD8+ T cell metabolism
T2  - Science
UR  - http://dx.doi.org/10.1126/science.aao4555
UR  - https://www.ncbi.nlm.nih.gov/pubmed/29724957
UR  - http://hdl.handle.net/10044/1/59092
VL  - 360
ER  -
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