Vessel wall adhesion
ICAM-1 leukocyte adhesion
Also searched as ICAM-1 leukocyte adhesion.
Immune cells travel in the blood, but to do damage they must cross into the tissue. This molecule is the grip that catches them as they pass. When it was turned down experimentally, inflammation in the heart fell with it — fewer grips, fewer invaders.
In depth
The molecular handhold that lets immune cells leave the blood and enter the heart muscle.
What drives it
Heart muscle inflammation increases it.
How the immune cells get out of the blood and into the muscle. Inflamed heart vessels put out a molecular grip that catches passing immune cells and lets them cross into the tissue. The direction was proved by turning it down: 'ETBR overexpression associated with ICAM-1 downregulation leads to inflammatory attenuation in experimental autoimmune myocarditis' (doi 10.7717/peerj.16320 (pmc10607261) — et-1 receptor type b (etbr) overexpression associated with icam-1 downregulation leads to inflammatory attenuation in experimental autoimmune myocarditis), with IFN-γ, IL-12 and IL-17 falling alongside it. ⇒ fewer grips, fewer invaders, less damage. doi 10.7717/peerj.16320
Viral entry receptor increases it.
PMC6881322 — The virus's doorway has a second job, and it works without any virus at all. Japanese work on the autoimmune model found: '心筋ミオシン免疫のみで心筋細胞および血管内皮においてCXADR発現が誘発されその後持続する' — cardiac myosin immunization alone induces cxadr expression in cardiomyocytes and vascular endothelium, and it persists. And: 'CXADR過剰発現マウスでは、コクサッキーウイルスが感染していなくても心筋組織への炎症細胞浸潤が認められた' — in mice overexpressing it, inflammatory cells infiltrated the heart even without any coxsackievirus infection (上原記念生命科学財団研究報告集 33 (2019) — EAMにおけるCXADR発現の解析 (Uehara Memorial Foundation Research Report Vol.33, Yokohama City University)). ⇒ the mechanism is adhesion: the endothelial cxadr domain 'JAMLと異種間分子結合を形成することで、循環免疫細胞の血管内皮への遊走・接着' — it binds jaml on circulating immune cells and pulls them into the vessel wall. the same protein that lets the virus in also lets the immune system in. It is a doorway in both directions, and the source calls it '劇症型心筋炎および心筋症に対する有力な治療標的の一つ' — a promising therapeutic target for fulminant myocarditis and cardiomyopathy. PMC6881322
What it drives
It increases Immune balance.
How the immune cells get out of the blood and into the muscle. Inflamed heart vessels put out a molecular grip that catches passing immune cells and lets them cross into the tissue. The direction was proved by turning it down: 'ETBR overexpression associated with ICAM-1 downregulation leads to inflammatory attenuation in experimental autoimmune myocarditis' (doi 10.7717/peerj.16320 (pmc10607261) — et-1 receptor type b (etbr) overexpression associated with icam-1 downregulation leads to inflammatory attenuation in experimental autoimmune myocarditis), with IFN-γ, IL-12 and IL-17 falling alongside it. ⇒ fewer grips, fewer invaders, less damage. doi 10.7717/peerj.16320
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.