Autoimmunity in the brain: The pathogenesis insight from cell biology
Само за регистроване кориснике
2007
Конференцијски прилог (Објављена верзија)
Метаподаци
Приказ свих података о документуАпстракт
The aim of the study is to explore the relationship between leakage of the blood-brain barrier and inflammation, the reason why demyelination occurs - seemingly in the absence of an antigen-specific immune response that requires explanation if a coherent account of an inflammatory-mediated demyelination is to be achieved. In this study the cellular biology of the glial cells important for the synthesis and maintenance of central nervous system (CNS) myelin and their inter-relations with other environmental cells (neuronal, microglial, olygodendroglial, astrocytes, endothelial, epithelial, T lymphocytes, B lymphocytes, monocytes, and macrophages) and with the compound of the extracellular matrix (ECM) during the development of an autoimmune inflammatory and demyelinating processes in the brain was analyzed. Upon activation in the peripheral tissue, immune cells reach their target organ via bloodstream and interacting with blood vessels wall components in the absence of exogenous stimulu...s mount an attack against the local milleu, which is the starting point of a pathogenic inflammatory reaction. Each of these contacts may trigger profuse secretion of cytokines, chemokines, and other soluble inflammatory mediators, which in the CNS by activating of local glial cells and by attracting and stimulating blood-borne monocyte/macrophages can act directly on neural cells and will cause their demyelination.
Кључне речи:
Autoimmune brain inflammation / Inflammatory demyelination / Neuroimmune interactionsИзвор:
Annals of the New York Academy of Sciences, 2007, 1107, 142-154Издавач:
- Blackwell Publishing Inc.
DOI: 10.1196/annals.1381.016
ISSN: 0077-8923
PubMed: 17804542
Scopus: 2-s2.0-34648814431
Институција/група
TorlakTY - CONF AU - Jovanova-Nešić, Katica AU - Shoenfeld, Yehuda PY - 2007 UR - http://intor.torlakinstitut.com/handle/123456789/237 AB - The aim of the study is to explore the relationship between leakage of the blood-brain barrier and inflammation, the reason why demyelination occurs - seemingly in the absence of an antigen-specific immune response that requires explanation if a coherent account of an inflammatory-mediated demyelination is to be achieved. In this study the cellular biology of the glial cells important for the synthesis and maintenance of central nervous system (CNS) myelin and their inter-relations with other environmental cells (neuronal, microglial, olygodendroglial, astrocytes, endothelial, epithelial, T lymphocytes, B lymphocytes, monocytes, and macrophages) and with the compound of the extracellular matrix (ECM) during the development of an autoimmune inflammatory and demyelinating processes in the brain was analyzed. Upon activation in the peripheral tissue, immune cells reach their target organ via bloodstream and interacting with blood vessels wall components in the absence of exogenous stimulus mount an attack against the local milleu, which is the starting point of a pathogenic inflammatory reaction. Each of these contacts may trigger profuse secretion of cytokines, chemokines, and other soluble inflammatory mediators, which in the CNS by activating of local glial cells and by attracting and stimulating blood-borne monocyte/macrophages can act directly on neural cells and will cause their demyelination. PB - Blackwell Publishing Inc. C3 - Annals of the New York Academy of Sciences T1 - Autoimmunity in the brain: The pathogenesis insight from cell biology EP - 154 SP - 142 VL - 1107 DO - 10.1196/annals.1381.016 ER -
@conference{ author = "Jovanova-Nešić, Katica and Shoenfeld, Yehuda", year = "2007", abstract = "The aim of the study is to explore the relationship between leakage of the blood-brain barrier and inflammation, the reason why demyelination occurs - seemingly in the absence of an antigen-specific immune response that requires explanation if a coherent account of an inflammatory-mediated demyelination is to be achieved. In this study the cellular biology of the glial cells important for the synthesis and maintenance of central nervous system (CNS) myelin and their inter-relations with other environmental cells (neuronal, microglial, olygodendroglial, astrocytes, endothelial, epithelial, T lymphocytes, B lymphocytes, monocytes, and macrophages) and with the compound of the extracellular matrix (ECM) during the development of an autoimmune inflammatory and demyelinating processes in the brain was analyzed. Upon activation in the peripheral tissue, immune cells reach their target organ via bloodstream and interacting with blood vessels wall components in the absence of exogenous stimulus mount an attack against the local milleu, which is the starting point of a pathogenic inflammatory reaction. Each of these contacts may trigger profuse secretion of cytokines, chemokines, and other soluble inflammatory mediators, which in the CNS by activating of local glial cells and by attracting and stimulating blood-borne monocyte/macrophages can act directly on neural cells and will cause their demyelination.", publisher = "Blackwell Publishing Inc.", journal = "Annals of the New York Academy of Sciences", title = "Autoimmunity in the brain: The pathogenesis insight from cell biology", pages = "154-142", volume = "1107", doi = "10.1196/annals.1381.016" }
Jovanova-Nešić, K.,& Shoenfeld, Y.. (2007). Autoimmunity in the brain: The pathogenesis insight from cell biology. in Annals of the New York Academy of Sciences Blackwell Publishing Inc.., 1107, 142-154. https://doi.org/10.1196/annals.1381.016
Jovanova-Nešić K, Shoenfeld Y. Autoimmunity in the brain: The pathogenesis insight from cell biology. in Annals of the New York Academy of Sciences. 2007;1107:142-154. doi:10.1196/annals.1381.016 .
Jovanova-Nešić, Katica, Shoenfeld, Yehuda, "Autoimmunity in the brain: The pathogenesis insight from cell biology" in Annals of the New York Academy of Sciences, 1107 (2007):142-154, https://doi.org/10.1196/annals.1381.016 . .