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Autoimmunity in acute ischemic stroke and the role of blood—brain barrier: the dark side or the light

Nikolay V. Tsygan, Alexandr P. Trashkov, Igor V. Litvinenko, Viktoriya A. Yakovleva, Alexandr V. Ryabtsev, Andrey G. Vasiliev, Leonid P. Churilov

Frontiers of Medicine 2019, Volume 13, Issue 4, Pages 420-426 doi: 10.1007/s11684-019-0688-6

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.

Keywords： stroke blood–brain barrier autoimmunity innate immunity inflammation cell death

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Chimeric Antigen Receptors and Regulatory T Cells: The Potential for HLA-Specific Immunosuppression in Transplantation Review

Sabrina Wright, Conor Hennessy, Joanna Hester, Fadi Issa

Engineering 2022, Volume 10, Issue 3, Pages 30-43 doi: 10.1016/j.eng.2021.10.018

Abstract:

Chimeric antigen receptors (CARs) are a breakthrough in genetic engineering that have revolutionized the field of adoptive cellular therapy (ACT). Cells expressing these receptors are rerouted to a predefined target by the inclusion of an antigen-specific binding region within the synthetic CAR construct. The advantage of cells with programmed specificity has been demonstrated clinically in the field of oncology, and it is clear that such cells have greater accuracy, potency, and reduced off-target therapeutic effects compared with their unmodified counterparts. In contrast to conventional T cells (Tconvs), regulatory T cells (Tregs) play a major role in suppressing immune activation and regulating the host immune response. CAR expression within Tregs has been proposed as a therapy for autoimmune and inflammatory diseases, graft-versus-host disease (GvHD), and organ transplant rejection. In the latter, they hold immense potential as mediators of immune tolerance for recipients of allotransplants. However, current research into CAR-Treg engineering is extremely limited, and there is uncertainty regarding optimal design for therapeutic use. This review examines the rationale behind the development of CAR-Tregs, their significance for human transplantation, potential designs, safety considerations, and comparisons of CAR-Tregs in transplantation models to date.

Keywords： Chimeric antigen receptors T cell Treg Alloimmunity Bioengineering Transplant Autoimmunity