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1.
Mol Biol (Mosk) ; 53(5): 790-798, 2019.
Artículo en Ruso | MEDLINE | ID: mdl-31661478

RESUMEN

Recently, much attention has been drawn to unraveling the mechanisms of neurodegenerative and neuroinflammatory disease pathogenesis. A special role in the development of neuropathologies is assigned to the interaction of the nervous and the immune systems. Microglia are the cells of the immune system that function as resident macrophages of the central nervous system (CNS) and are involved in the development of CNS, as well as in homeostatic interactions. Impaired microglia can contribute to neuroinflammation and neurodegeneration. With the help of genome editing technologies, the main paradigms in the development and functions of microglia have been addressed. At the same time, an understanding of the mechanisms of regulation of microglia in normal and pathological conditions is necessary to create an effective therapy aimed at treating various neurological diseases. This review focuses on recent findings on the origin of microglia, its regulatory role in the central nervous system, as well as its contribution to the development of neuroinflammation.


Asunto(s)
Sistema Nervioso Central/citología , Sistema Nervioso Central/fisiología , Homeostasis , Inflamación/patología , Microglía/fisiología , Enfermedades Neurodegenerativas/patología , Sistema Nervioso Central/patología , Sistema Nervioso Central/fisiopatología , Humanos , Inflamación/fisiopatología , Microglía/citología , Microglía/patología , Enfermedades Neurodegenerativas/fisiopatología
2.
Biochemistry (Mosc) ; 83(9): 1089-1103, 2018 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-30472948

RESUMEN

Cytokines play a pivotal role in maintaining homeostasis of the immune system and in regulation of the immune response. Cytokine dysregulation is often associated with development of various pathological conditions, including autoimmunity. Recent studies have provided insights into the cytokine signaling pathways that are involved not only in pathogenesis of autoimmune neuroinflammatory disorders, such as multiple sclerosis, but also in neurodegenerative states, for example, Alzheimer's disease. Understanding the exact molecular mechanisms of disease pathogenesis and evaluation of relevant experimental animal models are necessary for development of effective therapeutic approaches.


Asunto(s)
Citocinas/metabolismo , Encefalomielitis Autoinmune Experimental/patología , Animales , Anticuerpos Monoclonales/uso terapéutico , Encefalomielitis Autoinmune Experimental/inmunología , Encefalomielitis Autoinmune Experimental/metabolismo , Humanos , Esclerosis Múltiple/tratamiento farmacológico , Esclerosis Múltiple/inmunología , Esclerosis Múltiple/patología , Enfermedades Neurodegenerativas/inmunología , Enfermedades Neurodegenerativas/metabolismo , Enfermedades Neurodegenerativas/patología , Neuronas/metabolismo , Transducción de Señal , Linfocitos T Colaboradores-Inductores/inmunología , Linfocitos T Colaboradores-Inductores/metabolismo
3.
Mol Biol (Mosk) ; 52(6): 963-974, 2018.
Artículo en Ruso | MEDLINE | ID: mdl-30633239

RESUMEN

Reverse genetics approach, involving genome editing, makes it possible not only to establish the nonredundant and unique functions of genes and their products, but also to construct animal models for biomedical research. Interleukin 6 (IL-6) is an important immunoregulatory and proinflammatory cytokine that differs from many related proteins in having a rather complicated signal transduction scheme. Apart from the multiple functions of IL-6, the most relevant biological problem of recent years was establishing what cells produce IL-6, in what form IL-6 is produced, what cells are recipients of the IL-6 signal, and what are the downstream events and physiological consequences of the IL-6 signaling cascade. Because IL-6 is involved in the pathogenesis of many diseases and is a drug target, understanding the mechanisms of its normal and pathogenic effects is important for the clinics. The review summarizes the recent data available in the field.


Asunto(s)
Interleucina-6/metabolismo , Genética Inversa , Transducción de Señal , Animales , Humanos , Interleucina-6/genética
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