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Apoptosis in brain-specific autoimmune disease

Recent neuropathological studies of experimental autoimmune encephalomyelitis have focused attention on the high number of cells in the lesions that show typical morphological features of apoptosis. Surprisingly, it has turned out that the vast majority of apoptotic cells are T lymphocytes and that...

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Detalles Bibliográficos
Autores principales: Bauer, Jan, Wekerle, Hartmut, Lassmann, Hans
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Published by Elsevier Ltd. 1995
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7135830/
https://www.ncbi.nlm.nih.gov/pubmed/8679129
http://dx.doi.org/10.1016/0952-7915(95)80057-3
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author Bauer, Jan
Wekerle, Hartmut
Lassmann, Hans
author_facet Bauer, Jan
Wekerle, Hartmut
Lassmann, Hans
author_sort Bauer, Jan
collection PubMed
description Recent neuropathological studies of experimental autoimmune encephalomyelitis have focused attention on the high number of cells in the lesions that show typical morphological features of apoptosis. Surprisingly, it has turned out that the vast majority of apoptotic cells are T lymphocytes and that they actually represent the antigen-specific T-cell population responsible for the induction of the disease. Taken together, these data suggest that clearance of autoimmune inflammation in the nervous system is accomplished by the destruction of the antigen-specific T-cell population within the lesions. This may explain the low level of central nervous system specific T-cell memory formation, as well as previously unexplained phenomena of ‘epitope spreading’, in autoimmune inflammation of the nervous system
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spelling pubmed-71358302020-04-08 Apoptosis in brain-specific autoimmune disease Bauer, Jan Wekerle, Hartmut Lassmann, Hans Curr Opin Immunol Article Recent neuropathological studies of experimental autoimmune encephalomyelitis have focused attention on the high number of cells in the lesions that show typical morphological features of apoptosis. Surprisingly, it has turned out that the vast majority of apoptotic cells are T lymphocytes and that they actually represent the antigen-specific T-cell population responsible for the induction of the disease. Taken together, these data suggest that clearance of autoimmune inflammation in the nervous system is accomplished by the destruction of the antigen-specific T-cell population within the lesions. This may explain the low level of central nervous system specific T-cell memory formation, as well as previously unexplained phenomena of ‘epitope spreading’, in autoimmune inflammation of the nervous system Published by Elsevier Ltd. 1995-12 2002-02-11 /pmc/articles/PMC7135830/ /pubmed/8679129 http://dx.doi.org/10.1016/0952-7915(95)80057-3 Text en Copyright © 1995 Published by Elsevier Ltd. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.
spellingShingle Article
Bauer, Jan
Wekerle, Hartmut
Lassmann, Hans
Apoptosis in brain-specific autoimmune disease
title Apoptosis in brain-specific autoimmune disease
title_full Apoptosis in brain-specific autoimmune disease
title_fullStr Apoptosis in brain-specific autoimmune disease
title_full_unstemmed Apoptosis in brain-specific autoimmune disease
title_short Apoptosis in brain-specific autoimmune disease
title_sort apoptosis in brain-specific autoimmune disease
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7135830/
https://www.ncbi.nlm.nih.gov/pubmed/8679129
http://dx.doi.org/10.1016/0952-7915(95)80057-3
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