Autoimmunity in acute ischemic stroke and the role of blood-brain barrier: the dark side or the light one?
10.1007/s11684-019-0688-6
- Author:
Nikolay V TSYGAN
1
;
Alexandr P TRASHKOV
1
;
Igor V LITVINENKO
2
;
Viktoriya A YAKOVLEVA
2
;
Alexandr V RYABTSEV
2
;
Andrey G VASILIEV
3
;
Leonid P CHURILOV
4
Author Information
1. Department of Molecular and Radiation Biophysics, B.P. Konstantinov Petersburg Nuclear Physics Institute, Gatchina, Leningrad Region, 188300, Russian Federation.
2. Department of Nervous Diseases, S.M. Kirov Military Medical Academy, Saint Petersburg, 194044, Russian Federation.
3. Department of Pathological Physiology with the Course of Immunopathology, Saint Petersburg State Pediatric Medical University, Saint Petersburg, Russian Federation.
4. Department of Pathology, Laboratory of the Mosaic of Autoimmunity, Saint Petersburg State University, Saint Petersburg, 199034, Russian Federation. elpach@mail.ru.
- Publication Type:Journal Article
- Keywords:
autoimmunity;
blood-brain barrier;
cell death;
inflammation;
innate immunity;
stroke
- From:
Frontiers of Medicine
2019;13(4):420-426
- CountryChina
- Language:English
-
Abstract:
This article presents a synopsis of the current data on the mechanisms of blood-brain barrier (BBB) alteration and autoimmune response in acute ischemic stroke. Most researchers confirm the relationship between the severity of immunobiochemical changes and clinical outcome of acute ischemic stroke. Ischemic stroke is accompanied by aseptic inflammation, which alters the brain tissue and exposes the co-stimulatory molecules of the immune system and the neuronal antigens. To date, BBB is not considered the border between the immune system and central nervous system, and the local immune subsystems are found within and behind the BBB. BBB disruption contributes to the leakage of brain autoantigens and induction of secondary autoimmune response to neuronal antigens and long-term inflammation. Glymphatic system function is altered and jeopardized both in hemorrhagic and ischemic stroke types. The receptors of innate immunity (toll-like receptor-2 and toll-like receptor-4) are also involved in acute ischemia-reperfusion injury. Immune response is related to the key processes of blood clotting and fibrinolysis. At the same time, the stroke-induced immune activation may promote reparation phenomena in the brain. Subsequent research on the reduction of the acute ischemic brain injury through the target regulation of the immune response is promising.
