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Abundant Intracellular IgG in Enterocytes and Endoderm Lacking FcRn

FcRn, a non-classical MHCI molecule, transports IgG from mother to young and regulates the rate of IgG degradation throughout life. Brambell proposed a mechanism that unified these two functions, saying that IgG was pinocytosed nonspecifically by the cell into an FcRn-expressing endosome, where, at...

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Autores principales: Mohanty, Sudhasri, Kim, Jonghan, Ganesan, Latha P., Phillips, Gary S., Robinson, John M., Anderson, Clark L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3726603/
https://www.ncbi.nlm.nih.gov/pubmed/23923029
http://dx.doi.org/10.1371/journal.pone.0070863
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author Mohanty, Sudhasri
Kim, Jonghan
Ganesan, Latha P.
Phillips, Gary S.
Robinson, John M.
Anderson, Clark L.
author_facet Mohanty, Sudhasri
Kim, Jonghan
Ganesan, Latha P.
Phillips, Gary S.
Robinson, John M.
Anderson, Clark L.
author_sort Mohanty, Sudhasri
collection PubMed
description FcRn, a non-classical MHCI molecule, transports IgG from mother to young and regulates the rate of IgG degradation throughout life. Brambell proposed a mechanism that unified these two functions, saying that IgG was pinocytosed nonspecifically by the cell into an FcRn-expressing endosome, where, at low pH, it bound to FcRn and was exocytosed. This theory was immediately challenged by claims that FcRn specificity for ligand could be conferred at the cell surface in neonatal jejunum. Assessing Brambell's hypothesis we found abundant nonspecifically endocytosed IgG present in the cytoplasm of FcRn(−/−) enterocytes. Further, IgG was present in the intercellular clefts and the cores of FcRn(+/+) but not FcRn(−/−) jejunum. FcRn specificity for ligand could be determined within the cell.
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spelling pubmed-37266032013-08-06 Abundant Intracellular IgG in Enterocytes and Endoderm Lacking FcRn Mohanty, Sudhasri Kim, Jonghan Ganesan, Latha P. Phillips, Gary S. Robinson, John M. Anderson, Clark L. PLoS One Research Article FcRn, a non-classical MHCI molecule, transports IgG from mother to young and regulates the rate of IgG degradation throughout life. Brambell proposed a mechanism that unified these two functions, saying that IgG was pinocytosed nonspecifically by the cell into an FcRn-expressing endosome, where, at low pH, it bound to FcRn and was exocytosed. This theory was immediately challenged by claims that FcRn specificity for ligand could be conferred at the cell surface in neonatal jejunum. Assessing Brambell's hypothesis we found abundant nonspecifically endocytosed IgG present in the cytoplasm of FcRn(−/−) enterocytes. Further, IgG was present in the intercellular clefts and the cores of FcRn(+/+) but not FcRn(−/−) jejunum. FcRn specificity for ligand could be determined within the cell. Public Library of Science 2013-07-29 /pmc/articles/PMC3726603/ /pubmed/23923029 http://dx.doi.org/10.1371/journal.pone.0070863 Text en © 2013 Mohanty et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Mohanty, Sudhasri
Kim, Jonghan
Ganesan, Latha P.
Phillips, Gary S.
Robinson, John M.
Anderson, Clark L.
Abundant Intracellular IgG in Enterocytes and Endoderm Lacking FcRn
title Abundant Intracellular IgG in Enterocytes and Endoderm Lacking FcRn
title_full Abundant Intracellular IgG in Enterocytes and Endoderm Lacking FcRn
title_fullStr Abundant Intracellular IgG in Enterocytes and Endoderm Lacking FcRn
title_full_unstemmed Abundant Intracellular IgG in Enterocytes and Endoderm Lacking FcRn
title_short Abundant Intracellular IgG in Enterocytes and Endoderm Lacking FcRn
title_sort abundant intracellular igg in enterocytes and endoderm lacking fcrn
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3726603/
https://www.ncbi.nlm.nih.gov/pubmed/23923029
http://dx.doi.org/10.1371/journal.pone.0070863
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