Cardiac autoantibodies
Myocardial cross-reactive antibodies↓
Also searched as Myocardial cross-reactive antibodies.
Because the virus and the heart carry look-alike markers, some antibodies raised against the infection also bind the heart itself. These have been found in people with this illness and they predict who goes on to develop an enlarged, weakened heart — they have even been detected in relatives before symptoms appear. This is how a past infection keeps causing harm after the virus itself is gone.
In depth
Antibodies raised against the virus that also fit heart proteins.
What drives it
Immune balance reduces it.
The antibodies that mistake the heart for the virus — and predict what happens next. 'cross-reacting antibodies with auto-antigens have been found in patients with myocarditis and ARE indicative of progression to DCM', and cardiac auto-antibodies were shown to 'predict disease development in asymptomatic relatives' (pmc2519249 — Acute viral myocarditis). ⇒ this is the mechanism by which a past infection keeps damaging a heart long after the virus itself is gone.
Immune checkpoint reduces it.
And here is proof of the strongest kind for the autoantibody: transfer it alone, and the heart fails. 'autoantibodies against cardiac troponin i appeared in spontaneously developing autoimmune myocarditis in PD-1 deficient mice, who lack the T-cell receptor costimulatory molecule PD-1. The passive transfer of this antibody induced myocardial dysfunction. Later, this autoantibody was found in patients with myocarditis' (doi 10.1007/s00059-012-3692-z — Matsumori a. Lessons learned from experimental myocarditis, Herz 2012). ⇒ the antibody alone, with NO virus and NO immune cells, made the heart work worse — and the same antibody was then found in real patients. Troponin i is also the protein measured in a blood test when a heart is damaged. the marker and the target are the same molecule. doi 10.1007/s00059-012-3692-z
What it drives
It increases Heart muscle inflammation.
The antibodies that mistake the heart for the virus — and predict what happens next. 'cross-reacting antibodies with auto-antigens have been found in patients with myocarditis and ARE indicative of progression to DCM', and cardiac auto-antibodies were shown to 'predict disease development in asymptomatic relatives' (pmc2519249 — Acute viral myocarditis). ⇒ this is the mechanism by which a past infection keeps damaging a heart long after the virus itself is gone.
It increases Enlarged heart.
The antibodies that mistake the heart for the virus — and predict what happens next. 'cross-reacting antibodies with auto-antigens have been found in patients with myocarditis and ARE indicative of progression to DCM', and cardiac auto-antibodies were shown to 'predict disease development in asymptomatic relatives' (pmc2519249 — Acute viral myocarditis). ⇒ this is the mechanism by which a past infection keeps damaging a heart long after the virus itself is gone.
It reduces Heart muscle marker.
And here is proof of the strongest kind for the autoantibody: transfer it alone, and the heart fails. 'autoantibodies against cardiac troponin i appeared in spontaneously developing autoimmune myocarditis in PD-1 deficient mice, who lack the T-cell receptor costimulatory molecule PD-1. The passive transfer of this antibody induced myocardial dysfunction. Later, this autoantibody was found in patients with myocarditis' (doi 10.1007/s00059-012-3692-z — Matsumori a. Lessons learned from experimental myocarditis, Herz 2012). ⇒ the antibody alone, with NO virus and NO immune cells, made the heart work worse — and the same antibody was then found in real patients. Troponin i is also the protein measured in a blood test when a heart is damaged. the marker and the target are the same molecule. doi 10.1007/s00059-012-3692-z
Blends that modulate it
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