Surface-associated antigen induces permeabilization of primary mouse B-cells and lysosome exocytosis facilitating antigen uptake and presentation to T-cells

B-cell receptor (BCR)-mediated antigen internalization and presentation are essential for humoral memory immune responses. Antigen encountered by B-cells is often tightly associated with the surface of pathogens and/or antigen-presenting cells. Internalization of such antigens requires myosin-mediat...

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Autores principales:	Fernando Y Maeda, Jurriaan JH van Haaren, David B Langley, Daniel Christ, Norma W Andrews, Wenxia Song
Formato:	article
Lenguaje:	EN
Publicado:	eLife Sciences Publications Ltd 2021
Materias:	B cell surface antigen resealing lysosome endocytosis antigen presentation Medicine R Science Q Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/1c77923d23a442de8b9aa7e64904b956
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spelling	oai:doaj.org-article:1c77923d23a442de8b9aa7e64904b9562021-11-12T14:45:19ZSurface-associated antigen induces permeabilization of primary mouse B-cells and lysosome exocytosis facilitating antigen uptake and presentation to T-cells10.7554/eLife.669842050-084Xe66984https://doaj.org/article/1c77923d23a442de8b9aa7e64904b9562021-10-01T00:00:00Zhttps://elifesciences.org/articles/66984https://doaj.org/toc/2050-084XB-cell receptor (BCR)-mediated antigen internalization and presentation are essential for humoral memory immune responses. Antigen encountered by B-cells is often tightly associated with the surface of pathogens and/or antigen-presenting cells. Internalization of such antigens requires myosin-mediated traction forces and extracellular release of lysosomal enzymes, but the mechanism triggering lysosomal exocytosis is unknown. Here, we show that BCR-mediated recognition of antigen tethered to beads, to planar lipid-bilayers or expressed on cell surfaces causes localized plasma membrane (PM) permeabilization, a process that requires BCR signaling and non-muscle myosin II activity. B-cell permeabilization triggers PM repair responses involving lysosomal exocytosis, and B-cells permeabilized by surface-associated antigen internalize more antigen than cells that remain intact. Higher affinity antigens cause more B-cell permeabilization and lysosomal exocytosis and are more efficiently presented to T-cells. Thus, PM permeabilization by surface-associated antigen triggers a lysosome-mediated B-cell resealing response, providing the extracellular hydrolases that facilitate antigen internalization and presentation.Fernando Y MaedaJurriaan JH van HaarenDavid B LangleyDaniel ChristNorma W AndrewsWenxia SongeLife Sciences Publications LtdarticleB cellsurface antigenresealinglysosomeendocytosisantigen presentationMedicineRScienceQBiology (General)QH301-705.5ENeLife, Vol 10 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	B cell surface antigen resealing lysosome endocytosis antigen presentation Medicine R Science Q Biology (General) QH301-705.5
spellingShingle	B cell surface antigen resealing lysosome endocytosis antigen presentation Medicine R Science Q Biology (General) QH301-705.5 Fernando Y Maeda Jurriaan JH van Haaren David B Langley Daniel Christ Norma W Andrews Wenxia Song Surface-associated antigen induces permeabilization of primary mouse B-cells and lysosome exocytosis facilitating antigen uptake and presentation to T-cells
description	B-cell receptor (BCR)-mediated antigen internalization and presentation are essential for humoral memory immune responses. Antigen encountered by B-cells is often tightly associated with the surface of pathogens and/or antigen-presenting cells. Internalization of such antigens requires myosin-mediated traction forces and extracellular release of lysosomal enzymes, but the mechanism triggering lysosomal exocytosis is unknown. Here, we show that BCR-mediated recognition of antigen tethered to beads, to planar lipid-bilayers or expressed on cell surfaces causes localized plasma membrane (PM) permeabilization, a process that requires BCR signaling and non-muscle myosin II activity. B-cell permeabilization triggers PM repair responses involving lysosomal exocytosis, and B-cells permeabilized by surface-associated antigen internalize more antigen than cells that remain intact. Higher affinity antigens cause more B-cell permeabilization and lysosomal exocytosis and are more efficiently presented to T-cells. Thus, PM permeabilization by surface-associated antigen triggers a lysosome-mediated B-cell resealing response, providing the extracellular hydrolases that facilitate antigen internalization and presentation.
format	article
author	Fernando Y Maeda Jurriaan JH van Haaren David B Langley Daniel Christ Norma W Andrews Wenxia Song
author_facet	Fernando Y Maeda Jurriaan JH van Haaren David B Langley Daniel Christ Norma W Andrews Wenxia Song
author_sort	Fernando Y Maeda
title	Surface-associated antigen induces permeabilization of primary mouse B-cells and lysosome exocytosis facilitating antigen uptake and presentation to T-cells
title_short	Surface-associated antigen induces permeabilization of primary mouse B-cells and lysosome exocytosis facilitating antigen uptake and presentation to T-cells
title_full	Surface-associated antigen induces permeabilization of primary mouse B-cells and lysosome exocytosis facilitating antigen uptake and presentation to T-cells
title_fullStr	Surface-associated antigen induces permeabilization of primary mouse B-cells and lysosome exocytosis facilitating antigen uptake and presentation to T-cells
title_full_unstemmed	Surface-associated antigen induces permeabilization of primary mouse B-cells and lysosome exocytosis facilitating antigen uptake and presentation to T-cells
title_sort	surface-associated antigen induces permeabilization of primary mouse b-cells and lysosome exocytosis facilitating antigen uptake and presentation to t-cells
publisher	eLife Sciences Publications Ltd
publishDate	2021
url	https://doaj.org/article/1c77923d23a442de8b9aa7e64904b956
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Surface-associated antigen induces permeabilization of primary mouse B-cells and lysosome exocytosis facilitating antigen uptake and presentation to T-cells

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