Imperial College London
Alternate

ProfessorNadiaRosenthal

Faculty of Medicine, National Heart & Lung Institute

Chair in Cardiovascular Science&ScientificDirector
 
 
 
//

Contact

 

+44 (0)20 7594 2737n.rosenthal

 
 
//

Location

 

424W2ICTEM buildingHammersmith Campus

//

Summary

 

Publications

Citation

BibTex format

@unpublished{Sintou:2019:10.1101/542597,
author = {Sintou, A and Rifai, SE and Mansfield, C and Rothery, S and Sanchez, Alonso J and Narodden, S and Sharma, K and Ferraro, E and Hasham, M and Swiatlowska, P and Harding, S and Rosenthal, N and Gorelik, J and Sattler, S},
doi = {10.1101/542597},
publisher = {bioRxiv},
title = {Persistent anti-heart autoimmunity causes cardiomyocyte damage in chronic heart failure},
url = {http://dx.doi.org/10.1101/542597},
year = {2019}
}
Download

RIS format (EndNote, RefMan)

TY  - UNPB
AB  - Although clinicians and researchers have long appreciated the detrimental effects of excessive acute inflammation after myocardial infarction (MI), less is known about the role of the adaptive immune system in MI complications including heart failure. Yet, abundant cardiac self-antigens released from necrotic cardiomyocytes in a highly inflammatory environment are likely to overwhelm peripheral mechanisms of immunological self-tolerance and adaptive auto-reactivity against the heart may cause ongoing tissue destruction and exacerbate progression to chronic heart failure (CHF). Here, we confirm that the adaptive immune system is indeed persistently active in CHF due to ischemic heart disease triggered by MI in rats. Heart draining mediastinal lymph nodes contain active secondary follicles with mature class-switched IgG2a positive cells, and mature anti-heart auto-antibodies binding to cardiac epitopes are still present in serum as late as 16 weeks after MI. When applied to healthy cardiomyocytes in vitro, humoral factors present in CHF serum promoted apoptosis, cytotoxicity and signs of hypertrophy. These findings directly implicate post-MI autoimmunity as an integral feature of CHF progression, constituting a roadblock to effective regeneration and a promising target for therapeutic intervention.
AU  - Sintou,A
AU  - Rifai,SE
AU  - Mansfield,C
AU  - Rothery,S
AU  - Sanchez,Alonso J
AU  - Narodden,S
AU  - Sharma,K
AU  - Ferraro,E
AU  - Hasham,M
AU  - Swiatlowska,P
AU  - Harding,S
AU  - Rosenthal,N
AU  - Gorelik,J
AU  - Sattler,S
DO  - 10.1101/542597
PB  - bioRxiv
PY  - 2019///
TI  - Persistent anti-heart autoimmunity causes cardiomyocyte damage in chronic heart failure
UR  - http://dx.doi.org/10.1101/542597
UR  - https://doi.org/10.1101/542597
UR  - http://hdl.handle.net/10044/1/74125
ER  -
Download