Common immunopathogenesis of central nervous system diseases: the protein-homeostasis-system hypothesis
Abstract There are hundreds of central nervous system (CNS) diseases, but there are few diseases for which the etiology or pathogenesis is understood as well as those of other organ-specific diseases. Cells in the CNS are selectively protected from external and internal insults by the blood–brain ba...
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Format: | Article |
Language: | English |
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BMC
2022-11-01
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Series: | Cell & Bioscience |
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Online Access: | https://doi.org/10.1186/s13578-022-00920-5 |
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author | Kyung-Yil Lee |
author_facet | Kyung-Yil Lee |
author_sort | Kyung-Yil Lee |
collection | DOAJ |
description | Abstract There are hundreds of central nervous system (CNS) diseases, but there are few diseases for which the etiology or pathogenesis is understood as well as those of other organ-specific diseases. Cells in the CNS are selectively protected from external and internal insults by the blood–brain barrier. Thus, the neuroimmune system, including microglia and immune proteins, might control external or internal insults that the adaptive immune system cannot control or mitigate. The pathologic findings differ by disease and show a state of inflammation that reflects the relationship between etiological or inflammation-inducing substances and corresponding immune reactions. Current immunological concepts about infectious diseases and infection-associated immune-mediated diseases, including those in the CNS, can only partly explain the pathophysiology of disease because they are based on the idea that host cell injury is caused by pathogens. Because every disease involves etiological or triggering substances for disease-onset, the protein-homeostasis-system (PHS) hypothesis proposes that the immune systems in the host control those substances according to the size and biochemical properties of the substances. In this article, I propose a common immunopathogenesis of CNS diseases, including prion diseases, Alzheimer’s disease, and genetic diseases, through the PHS hypothesis. |
first_indexed | 2024-04-11T06:55:31Z |
format | Article |
id | doaj.art-3c5b41b4bb3c41d391bff83fb7359cbd |
institution | Directory Open Access Journal |
issn | 2045-3701 |
language | English |
last_indexed | 2024-04-11T06:55:31Z |
publishDate | 2022-11-01 |
publisher | BMC |
record_format | Article |
series | Cell & Bioscience |
spelling | doaj.art-3c5b41b4bb3c41d391bff83fb7359cbd2022-12-22T04:39:02ZengBMCCell & Bioscience2045-37012022-11-0112111510.1186/s13578-022-00920-5Common immunopathogenesis of central nervous system diseases: the protein-homeostasis-system hypothesisKyung-Yil Lee0The Catholic University of Korea College of MedicineAbstract There are hundreds of central nervous system (CNS) diseases, but there are few diseases for which the etiology or pathogenesis is understood as well as those of other organ-specific diseases. Cells in the CNS are selectively protected from external and internal insults by the blood–brain barrier. Thus, the neuroimmune system, including microglia and immune proteins, might control external or internal insults that the adaptive immune system cannot control or mitigate. The pathologic findings differ by disease and show a state of inflammation that reflects the relationship between etiological or inflammation-inducing substances and corresponding immune reactions. Current immunological concepts about infectious diseases and infection-associated immune-mediated diseases, including those in the CNS, can only partly explain the pathophysiology of disease because they are based on the idea that host cell injury is caused by pathogens. Because every disease involves etiological or triggering substances for disease-onset, the protein-homeostasis-system (PHS) hypothesis proposes that the immune systems in the host control those substances according to the size and biochemical properties of the substances. In this article, I propose a common immunopathogenesis of CNS diseases, including prion diseases, Alzheimer’s disease, and genetic diseases, through the PHS hypothesis.https://doi.org/10.1186/s13578-022-00920-5Central nervous system diseasesPathogenesisPrion diseasesAlzheimer diseaseGenetic diseasesProtein-homeostasis-system hypothesis |
spellingShingle | Kyung-Yil Lee Common immunopathogenesis of central nervous system diseases: the protein-homeostasis-system hypothesis Cell & Bioscience Central nervous system diseases Pathogenesis Prion diseases Alzheimer disease Genetic diseases Protein-homeostasis-system hypothesis |
title | Common immunopathogenesis of central nervous system diseases: the protein-homeostasis-system hypothesis |
title_full | Common immunopathogenesis of central nervous system diseases: the protein-homeostasis-system hypothesis |
title_fullStr | Common immunopathogenesis of central nervous system diseases: the protein-homeostasis-system hypothesis |
title_full_unstemmed | Common immunopathogenesis of central nervous system diseases: the protein-homeostasis-system hypothesis |
title_short | Common immunopathogenesis of central nervous system diseases: the protein-homeostasis-system hypothesis |
title_sort | common immunopathogenesis of central nervous system diseases the protein homeostasis system hypothesis |
topic | Central nervous system diseases Pathogenesis Prion diseases Alzheimer disease Genetic diseases Protein-homeostasis-system hypothesis |
url | https://doi.org/10.1186/s13578-022-00920-5 |
work_keys_str_mv | AT kyungyillee commonimmunopathogenesisofcentralnervoussystemdiseasestheproteinhomeostasissystemhypothesis |