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Recognition of major histocompatibility complexantigens on murine glial cells()

Recognition of autologous major histocompatibility complex (MHC) antigens by T cells is an essential step in the induction of an immunologic reaction to either endogenous or exogenous antigens. We investigated the ability of murine glial cells of different ages to stimulate clones of allospecific T...

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Detalles Bibliográficos
Autores principales: Birnbaum, Gary, Clinchy, Birgitta, Widmer, Michael B.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Published by Elsevier B.V. 1986
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7119635/
https://www.ncbi.nlm.nih.gov/pubmed/3488333
http://dx.doi.org/10.1016/S0165-5728(86)80006-6
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author Birnbaum, Gary
Clinchy, Birgitta
Widmer, Michael B.
author_facet Birnbaum, Gary
Clinchy, Birgitta
Widmer, Michael B.
author_sort Birnbaum, Gary
collection PubMed
description Recognition of autologous major histocompatibility complex (MHC) antigens by T cells is an essential step in the induction of an immunologic reaction to either endogenous or exogenous antigens. We investigated the ability of murine glial cells of different ages to stimulate clones of allospecific T lymphocytes. We also investigated the effects of supernatants from cultures of activated T cells on the immunologic recognition of MHC antigens on murine glial cells. Lymphocyte clones specific for Class I, Class II and non-MHC, background antigens were obtained from C57B1/6J-anti-DBA/2 mixed lymphocyte cultures. Glial cell cultures were prepared from newborn syngeneic (C57B1/6J) and allogeneic (DBA/2) mouse brains. Glial cultures 1–4 weeks of age were able to stimulate α-Class I-specific clones. No stimulation of α-Class II or α-background clones was noted. Incubation of glial cells with supernatants from cultures of alloantigen-activated spleen cells (C57131/0-anti-DBA/2) resulted in a decreased ability of glial cells to stimulate a-Class I responses. In contrast supernatant-treated cultures acquired the capacity to stimulate a-Class II-specific clones. No responses were noted in clones responsive to non-MHC antigens. The ability to stimulate α-Class II-specific clones was most prominent with one-week-old glial cultures and was lost by four weeks of culture. The increased susceptibility of younger glial cultures to the modulatory effects of lymphokines from activated T cells may be a factor in the increased susceptibility of the immature central nervous system to persistent viral infections and the development of autoimmune phenomena.
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spelling pubmed-71196352020-04-08 Recognition of major histocompatibility complexantigens on murine glial cells() Birnbaum, Gary Clinchy, Birgitta Widmer, Michael B. J Neuroimmunol Article Recognition of autologous major histocompatibility complex (MHC) antigens by T cells is an essential step in the induction of an immunologic reaction to either endogenous or exogenous antigens. We investigated the ability of murine glial cells of different ages to stimulate clones of allospecific T lymphocytes. We also investigated the effects of supernatants from cultures of activated T cells on the immunologic recognition of MHC antigens on murine glial cells. Lymphocyte clones specific for Class I, Class II and non-MHC, background antigens were obtained from C57B1/6J-anti-DBA/2 mixed lymphocyte cultures. Glial cell cultures were prepared from newborn syngeneic (C57B1/6J) and allogeneic (DBA/2) mouse brains. Glial cultures 1–4 weeks of age were able to stimulate α-Class I-specific clones. No stimulation of α-Class II or α-background clones was noted. Incubation of glial cells with supernatants from cultures of alloantigen-activated spleen cells (C57131/0-anti-DBA/2) resulted in a decreased ability of glial cells to stimulate a-Class I responses. In contrast supernatant-treated cultures acquired the capacity to stimulate a-Class II-specific clones. No responses were noted in clones responsive to non-MHC antigens. The ability to stimulate α-Class II-specific clones was most prominent with one-week-old glial cultures and was lost by four weeks of culture. The increased susceptibility of younger glial cultures to the modulatory effects of lymphokines from activated T cells may be a factor in the increased susceptibility of the immature central nervous system to persistent viral infections and the development of autoimmune phenomena. Published by Elsevier B.V. 1986-09 2005-03-07 /pmc/articles/PMC7119635/ /pubmed/3488333 http://dx.doi.org/10.1016/S0165-5728(86)80006-6 Text en Copyright © 1986 Published by Elsevier B.V. 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
Birnbaum, Gary
Clinchy, Birgitta
Widmer, Michael B.
Recognition of major histocompatibility complexantigens on murine glial cells()
title Recognition of major histocompatibility complexantigens on murine glial cells()
title_full Recognition of major histocompatibility complexantigens on murine glial cells()
title_fullStr Recognition of major histocompatibility complexantigens on murine glial cells()
title_full_unstemmed Recognition of major histocompatibility complexantigens on murine glial cells()
title_short Recognition of major histocompatibility complexantigens on murine glial cells()
title_sort recognition of major histocompatibility complexantigens on murine glial cells()
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7119635/
https://www.ncbi.nlm.nih.gov/pubmed/3488333
http://dx.doi.org/10.1016/S0165-5728(86)80006-6
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