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Type: Original Article
Title: A study on Mer- tyrosine kinase (MerTK)
Authors: Ertugrul Kilic
Affiliations: Department of Physiology, Faculty of Medicine, Istanbul Medipol University, Istanbul 34810, Turkey.
Abstract: MerTK three receptor kinase, Tyro3, Axl and Mer (TAM) and their ligands Gas6 and Protein S, are robust negative regulators of innate immune response. In a series of studies in which TAM locus is genetically removed from mice, functional mechanisms of TAM receptors in the development of immune response and phagocytosis of apoptotic cells were investigated. After the phagocytosis of apoptotic cells and induction of T cell-dependent adaptive immune response, ligand-dependent TAM signals inhibit long-term inflammation by reducing the proinflammatory cytokine production. MerTK has the highest affinity in phagocytotic processes among the TAM family. Even though it is well-known that MerTK plays a role in phagocytosis of apoptotic cells in the brain and other tissues, the knowledge regarding the pathophysiological processes following brain injury is limited and there is a huge demand in the literature about this issue. To this end, we are planning to investigate the role of MerTK in the reorganization of the brain following brain injury.
Title: Resolution of inflammation and repair after ischemic brain injury
Authors: Akihiko Yoshimura1, Minako Ito1,2
Affiliations: 1Department of Microbiology and Immunology, Keio University School of Medicine, Tokyo 160-8582, Japan.
2Division of Allergy and Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan.
Abstract: After ischemic stroke, the proinflammatory molecules known as DAMPs (danger-associated molecular patterns), secreted by damaged brain cells, recruit and activate immune cells (neutrophils, macrophages, and lymphocytes) and elicit innate and adaptive immunity. During the acute phase, from Day 1 to Day 3 after stroke onset, macrophages play major roles in the progression of inflammation, which promotes the destruction of brain tissue. During the recovery phase, from Days 3-4 to Day 7 after stroke onset, the infiltrating macrophages switch to repairing macrophages, which clear the DAMPs and promote tissue repair by producing neurotrophic factors. Adaptive immunity during the late or chronic phase (> Day 7) of stroke has not been well investigated. However, recent studies have indicated that antigen-specific T cells, especially regulatory T cells (Tregs), play major roles in neural repair. This review mostly focuses on the resolution of inflammation and tissue repair by macrophages and Tregs.
Title: Microglial response after brain stroke
Authors: Olivier Wurtz
Affiliations: Institut de Recherche et d'Innovation Biomédicale (IRIB), Université de Rouen, Rouen 76821, France.
Abstract: Despite years of intense research, brain stroke remains a leading cause of death and long-term disabilities worldwide. Acute ischemic stroke, the most prevalent stroke subtype, results from a thrombus responsible for the sudden blockage of blood flow in a given cerebral territory. The breakdown of oxygen and nutrients supply initiates a cascade of pathophysiological events evolving in time and space, leading to a massive neuronal cell death and consecutive neurological deficits. Among the post-ischemic mechanisms, inflammation is a complex process initiated early after stroke onset and sustained over weeks, exerting both detrimental and beneficial effects. Microglial cell population, a unique immunocompetent compartment in the brain parenchyma, tightly controls the neuroinflammatory response and becomes an interesting therapeutical target. Initially thought to increase neuronal cell death through proinflammatory mediator secretion and reactive species production, numerous studies also report the neuroprotective role of microglia promoting neuronal trophic support and tissue repair. Hence, the phenotype of the microglial response can evolve according to environmental cues and timing after brain injury. Here, we focus on the duality of this microglial response, its versatility and dynamic in relation with the evolution of signals available during the different phases of the disease. We discuss the relationships between the phenotype of the microglial response and the cellular processes, which can support detrimental and beneficial consequences. Understanding the signals that drive microglial cell polarization will allow the development of therapeutical strategies designed to skew, rather than simply inhibiting, the post-ischemic microglial response toward its neuroprotective phenotype. Definitely, such immunomodulatory strategies targeting microglial responses in the early phase as well as in the late phase of stroke could contribute to improving functional recovery in stroke victims.