B1 Cell IgE Impedes Mast Cell-Mediated Enhancement of Parasite Expulsion through B2 IgE Blockade
Summary: Helminth infection is known for generating large amounts of poly-specific IgE. Here we demonstrate that innate-like B1 cells are responsible for this IgE production during infection with the nematode parasites Nippostrongylus brasiliensis and Heligmosomoides polygyrus bakeri. In vitro analy...
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doaj-f4577ef0704b41a9a257d4dd0468027d2020-11-25T03:49:23ZengElsevierCell Reports2211-12472018-02-012271824183410.1016/j.celrep.2018.01.048B1 Cell IgE Impedes Mast Cell-Mediated Enhancement of Parasite Expulsion through B2 IgE BlockadeRebecca K. Martin0Sheela R. Damle1Yolander A. Valentine2Matthew P. Zellner3Briana N. James4Joseph C. Lownik5Andrea J. Luker6Elijah H. Davis7Martha M. DeMeules8Laura M. Khandjian9Fred D. Finkelman10Joseph F. Urban, Jr.11Daniel H. Conrad12Department of Microbiology and Immunology, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298, USADepartment of Microbiology and Immunology, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298, USADepartment of Microbiology and Immunology, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298, USADepartment of Microbiology and Immunology, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298, USADepartment of Microbiology and Immunology, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298, USADepartment of Microbiology and Immunology, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298, USA; Center for Clinical and Translational Research, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298, USADepartment of Microbiology and Immunology, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298, USADepartment of Microbiology and Immunology, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298, USADepartment of Microbiology and Immunology, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298, USA; University of Wisconsin-Madison, Madison, WI 53715, USADepartment of Microbiology and Immunology, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298, USADivision of Immunology, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA; Medicine Service, Veterans Administration Medical Center, Cincinnati, OH, USAUnited States Department of Agriculture, Agricultural Research Service, Diet, Genomics and Immunology Laboratory, Beltsville, MD 20705, USADepartment of Microbiology and Immunology, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298, USA; Corresponding authorSummary: Helminth infection is known for generating large amounts of poly-specific IgE. Here we demonstrate that innate-like B1 cells are responsible for this IgE production during infection with the nematode parasites Nippostrongylus brasiliensis and Heligmosomoides polygyrus bakeri. In vitro analysis of B1 cell immunoglobulin class switch recombination to IgE demonstrated a requirement for anti-CD40 and IL-4 that was further enhanced when IL-5 was added or when the B1 source was helminth infected mice. An IL-25-induced upregulation of IgE in B1 cells was also demonstrated. In T cell-reconstituted RAG1−/− mice, N. brasiliensis clearance was enhanced with the addition of B2 cells in an IgE-dependent manner. This enhanced clearance was impeded by reconstitution with IgE sufficient B1 cells. Mucosal mast cells mediated the B2 cell enhancement of clearance in the absence of B1 cells. The data support B1 cell IgE secretion as a regulatory response exploited by the helminth.http://www.sciencedirect.com/science/article/pii/S2211124718300809helminthB1 cellsB2 cellsmast cellsTh2N. brasiliensis |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Rebecca K. Martin Sheela R. Damle Yolander A. Valentine Matthew P. Zellner Briana N. James Joseph C. Lownik Andrea J. Luker Elijah H. Davis Martha M. DeMeules Laura M. Khandjian Fred D. Finkelman Joseph F. Urban, Jr. Daniel H. Conrad |
spellingShingle |
Rebecca K. Martin Sheela R. Damle Yolander A. Valentine Matthew P. Zellner Briana N. James Joseph C. Lownik Andrea J. Luker Elijah H. Davis Martha M. DeMeules Laura M. Khandjian Fred D. Finkelman Joseph F. Urban, Jr. Daniel H. Conrad B1 Cell IgE Impedes Mast Cell-Mediated Enhancement of Parasite Expulsion through B2 IgE Blockade Cell Reports helminth B1 cells B2 cells mast cells Th2 N. brasiliensis |
author_facet |
Rebecca K. Martin Sheela R. Damle Yolander A. Valentine Matthew P. Zellner Briana N. James Joseph C. Lownik Andrea J. Luker Elijah H. Davis Martha M. DeMeules Laura M. Khandjian Fred D. Finkelman Joseph F. Urban, Jr. Daniel H. Conrad |
author_sort |
Rebecca K. Martin |
title |
B1 Cell IgE Impedes Mast Cell-Mediated Enhancement of Parasite Expulsion through B2 IgE Blockade |
title_short |
B1 Cell IgE Impedes Mast Cell-Mediated Enhancement of Parasite Expulsion through B2 IgE Blockade |
title_full |
B1 Cell IgE Impedes Mast Cell-Mediated Enhancement of Parasite Expulsion through B2 IgE Blockade |
title_fullStr |
B1 Cell IgE Impedes Mast Cell-Mediated Enhancement of Parasite Expulsion through B2 IgE Blockade |
title_full_unstemmed |
B1 Cell IgE Impedes Mast Cell-Mediated Enhancement of Parasite Expulsion through B2 IgE Blockade |
title_sort |
b1 cell ige impedes mast cell-mediated enhancement of parasite expulsion through b2 ige blockade |
publisher |
Elsevier |
series |
Cell Reports |
issn |
2211-1247 |
publishDate |
2018-02-01 |
description |
Summary: Helminth infection is known for generating large amounts of poly-specific IgE. Here we demonstrate that innate-like B1 cells are responsible for this IgE production during infection with the nematode parasites Nippostrongylus brasiliensis and Heligmosomoides polygyrus bakeri. In vitro analysis of B1 cell immunoglobulin class switch recombination to IgE demonstrated a requirement for anti-CD40 and IL-4 that was further enhanced when IL-5 was added or when the B1 source was helminth infected mice. An IL-25-induced upregulation of IgE in B1 cells was also demonstrated. In T cell-reconstituted RAG1−/− mice, N. brasiliensis clearance was enhanced with the addition of B2 cells in an IgE-dependent manner. This enhanced clearance was impeded by reconstitution with IgE sufficient B1 cells. Mucosal mast cells mediated the B2 cell enhancement of clearance in the absence of B1 cells. The data support B1 cell IgE secretion as a regulatory response exploited by the helminth. |
topic |
helminth B1 cells B2 cells mast cells Th2 N. brasiliensis |
url |
http://www.sciencedirect.com/science/article/pii/S2211124718300809 |
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