The "gatedog" of small glial cells in the olfactory ball protects the brain from infection.

Introduction: Recently, researchers from the National Institute of neurological diseases and stroke (NINDS) of the National Institutes of Health (NIH) have identified a specific first-line defense measure that can limit the infection to the olfactory bulb and protect the neurons of the olfactory bulb from infection.the study was published in scientific immunology.neurons in the nose respond to inhaled odors and send this information to an area of the brain called the olfactory bulb.although the location of nasal neurons and their exposure to the external environment make them easy targets for airborne viral infections, viral respiratory infections rarely spread from the olfactory bulb to other parts of the brain that could cause fatal encephalitis.airborne viruses have been challenging the immune system, but it is rarely seen that virus infection leads to nervous system diseases.this means that the immune system in this region must be very good at protecting the brain.more experiments show that immune cells and microglia in the central nervous system do not play a role in helping the immune system to recognize viruses, and to some extent limit the damage of neurons themselves.it is important to retain neurons because, unlike cells in most other tissues, most neuronal populations do not recover.therefore, the central nervous system has evolved a variety of defense mechanisms to resist pathogens.however, after inhaling airborne viruses, they pass through the nasal cavity and interact with the olfactory epithelial tissue responsible for olfactory function.neurons at the edge of the olfactory system extend through the bone layer of the nasal cavity and extend small processes.these projections enter the brain, exposing the brain to air odors.neurons in olfactory epithelial cells also provide a direct access to the brain, providing a simple way for viruses to bypass the traditional central nervous system disorders.if the virus infects neurons suspended in the respiratory tract, the virus may enter the brain and eventually cause encephalitis or meningitis.the researchers expressed interest in understanding the immune response at the interface between olfactory neurons at the end of the olfactory bulb and the rest of the brain.researchers led by Dr. Dorian mcgavenn, a senior researcher at NINDS, have found that CD8 T cells are part of the immune system responsible for controlling the virus and are important for protecting the brain after nasal infection.mcgarvin's team used advanced fluorescence microscopy to observe in real time how CD8 T cells protect the brain from rhinovirus infection. interestingly, CD8 T cells do not seem to interact directly with the neurons of the main infected cell population. on the contrary, they are in contact with microglia, which are immune cells of the central nervous system and act like garbage collectors by removing cell debris and dead cell substances. when a viral infection occurs, microglia seem to absorb viral substances from the surrounding environment and present them to the immune system as if they had been infected. in this way, infected olfactory neurons can "deliver" viral particles to microglia, which can then be detected by T cells. then, T cells react by releasing antiviral molecules, thereby eliminating the virus from neurons in a way that does not kill the cells. because microglia are renewable cell types, this interaction is meaningful from an evolutionary point of view. the immune system has developed strategies to preserve neurons at all costs. this study demonstrates that microglia can "absorb shocks" from neurons by involving T cells, and then make antiviral programs work. due to the current covid-19 pandemic, respiratory virus infection has attracted great attention recently. Dr. mcgarvin pointed out that although the virus was not studied in these experiments, some of the symptoms it produces suggest that the same mechanisms described here may be working. The novel coronavirus infection associated with is one of the interesting symptoms of many people who lose their sense of smell and taste. this indicates that the virus is not only a respiratory pathogen, but also may target or destroy olfactory sensory neurons. it is worth noting that widespread infection of olfactory sensory neurons, whether new coronavirus, virus used in this study or any other virus like infection, may destroy people's sense of smell. however, unlike other neurons in the central nervous system, these start in the nose and end up in the brain where sensory neurons regenerate after clearing the infection. moreover, the immune response described by the researchers did not protect olfactory sensory neurons nor olfactory sensory neurons. this is not necessarily a long-term problem, as these sensory neurons can be replaced once the virus is treated. the key is to protect the brain and central nervous system from encephalitis or meningitis. Human olfactory function can be restored over time. and given the importance of microglia in stimulating antiviral responses, factors that may lead to their depletion or loss of function may increase the susceptibility to central nervous system infection. Ref: moseman, EA et al. T cell engagement of cross presenting microglia protection the brain from nasal virus infection. Science immunology. June 5, 2020. Doi: 10.1126/ sciimmunol.abb1817 Recommended reading: fight against epidemic situation, translational medical network content team series report: [Nature] bald star people leave moving tears! New breakthrough in regenerative medicine! [heavyweight] data support for the first time: fragmented sleep is harmful! Can lead to chronic inflammation and atherosclerosis [Nature] new progress: too much pressure to carry? It's true! Excessive pressure will cause a large number of inflammatory reactions in the human body! Near infrared light stimulation can restore vision! 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