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pubmed-2187244
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| recordtype |
oai_dc
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pubmed-21872442008-04-17 Dichotomy in the tissue origin of schistosome acquired class I and class II major histocompatibility complex antigens Articles Schistosoma mansoni schistosomula recovered from the lungs of mice have previously been shown to express host-derived class I and class II major histocompatibility complex (MHC) antigens. To investigate the tissue origin of parasite-acquired MHC products, lung-stage schistosomula were obtained from a series of parent leads to F1 and F1 leads to parent bone marrow chimeras and the parasites typed by immunofluorescence for the presence of haplotype-specific K region and I region MHC determinants. The results of these experiments indicated that, despite their intravascular residence in the host, schistosomula derive all of their class I antigen from a nonhemapoietic tissue source. In contrast, the class II antigens expressed on the surface of schistosomula were found to originate from bone marrow-derived donor cells. These results support the hypothesis that MHC product acquisition by schistosomes involves selective and specific interactions with host tissue and, in the case of class I antigens, suggest that the endothelium may be a major site of host molecule uptake for the parasite. The Rockefeller University Press 1984-03-01 /pmc/articles/PMC2187244/ /pubmed/6366108 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
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| repository_type |
Open Access Journal
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| institution_category |
Foreign Institution
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| institution |
US National Center for Biotechnology Information
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| building |
NCBI PubMed
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| collection |
Online Access
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| language |
English
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| format |
Online
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| title |
Dichotomy in the tissue origin of schistosome acquired class I and class II major histocompatibility complex antigens
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| spellingShingle |
Dichotomy in the tissue origin of schistosome acquired class I and class II major histocompatibility complex antigens
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| title_short |
Dichotomy in the tissue origin of schistosome acquired class I and class II major histocompatibility complex antigens
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| title_full |
Dichotomy in the tissue origin of schistosome acquired class I and class II major histocompatibility complex antigens
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| title_fullStr |
Dichotomy in the tissue origin of schistosome acquired class I and class II major histocompatibility complex antigens
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| title_full_unstemmed |
Dichotomy in the tissue origin of schistosome acquired class I and class II major histocompatibility complex antigens
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| title_sort |
dichotomy in the tissue origin of schistosome acquired class i and class ii major histocompatibility complex antigens
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| description |
Schistosoma mansoni schistosomula recovered from the lungs of mice have previously been shown to express host-derived class I and class II major histocompatibility complex (MHC) antigens. To investigate the tissue origin of parasite-acquired MHC products, lung-stage schistosomula were obtained from a series of parent leads to F1 and F1 leads to parent bone marrow chimeras and the parasites typed by immunofluorescence for the presence of haplotype-specific K region and I region MHC determinants. The results of these experiments indicated that, despite their intravascular residence in the host, schistosomula derive all of their class I antigen from a nonhemapoietic tissue source. In contrast, the class II antigens expressed on the surface of schistosomula were found to originate from bone marrow-derived donor cells. These results support the hypothesis that MHC product acquisition by schistosomes involves selective and specific interactions with host tissue and, in the case of class I antigens, suggest that the endothelium may be a major site of host molecule uptake for the parasite.
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| publisher |
The Rockefeller University Press
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| publishDate |
1984
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| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2187244/
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| _version_ |
1611427622353371136
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