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Secreted IgD Amplifies Humoral T Helper 2 Cell Responses by Binding Basophils via Galectin-9 and CD44.

  • Shan M Department of Medicine, Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Mucosal Immunology Studies Team (MIST), National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20982, USA.
  • Carrillo J Department of Medicine, Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Institut de Recerca de la SIDA-IrsiCaixa-HIVACAT, IGTP, UAB, 08916 Badalona, Barcelona, Spain.
  • Yeste A Program for Inflammatory and Cardiovascular Disorders, Institut Hospital del Mar d'Investigacions Mèdiques (IMIM), 08003 Barcelona, Spain.
  • Gutzeit C Department of Medicine, Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
  • Segura-Garzón D Program for Inflammatory and Cardiovascular Disorders, Institut Hospital del Mar d'Investigacions Mèdiques (IMIM), 08003 Barcelona, Spain.
  • Walland AC Department of Medicine, Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
  • Pybus M Program for Inflammatory and Cardiovascular Disorders, Institut Hospital del Mar d'Investigacions Mèdiques (IMIM), 08003 Barcelona, Spain.
  • Grasset EK Department of Medicine, Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Department of Medicine, Center for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital, 171 77 Stockholm, Sweden.
  • Yeiser JR Department of Medicine, Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
  • Matthews DB Department of Medicine, Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
  • van de Veen W Swiss Institute of Allergy and Asthma Research, University of Zurich, Christine-Kühne Research Center for Allergy and Education, 7270 Davos, Switzerland.
  • Comerma L Program for Inflammatory and Cardiovascular Disorders, Institut Hospital del Mar d'Investigacions Mèdiques (IMIM), 08003 Barcelona, Spain.
  • He B Department of Medicine, Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
  • Boonpiyathad T Swiss Institute of Allergy and Asthma Research, University of Zurich, Christine-Kühne Research Center for Allergy and Education, 7270 Davos, Switzerland.
  • Lee H Department of Medicine, Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
  • Blanco J Institut de Recerca de la SIDA-IrsiCaixa-HIVACAT, IGTP, UAB, 08916 Badalona, Barcelona, Spain; University of Vic, UVIC-UCC, 08500 Vic, Barcelona, Spain.
  • Osborne LC Department of Medicine, Jill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Medical College of Cornell University, New York, NY 10021, USA.
  • Siracusa MC Department of Medicine, Center for Immunity and Inflammation, Rutgers New Jersey Medical School, Newark, NJ 07103, USA.
  • Akdis M Swiss Institute of Allergy and Asthma Research, University of Zurich, Christine-Kühne Research Center for Allergy and Education, 7270 Davos, Switzerland.
  • Artis D Mucosal Immunology Studies Team (MIST), National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20982, USA; Department of Medicine, Jill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Medical College of Cornell University, New York, NY 10021, USA.
  • Mehandru S Department of Medicine, Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Department of Gastroenterology, Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
  • Sampson HA Division of Pediatric Allergy and Immunology, Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
  • Berin MC Division of Pediatric Allergy and Immunology, Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
  • Chen K Mucosal Immunology Studies Team (MIST), National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20982, USA; Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
  • Cerutti A Department of Medicine, Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Mucosal Immunology Studies Team (MIST), National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20982, USA; Program for Inflammatory and Cardiovascular Disorders, Institut Hospital del Mar d'Investigacions Mèdiques (IMIM), 08003 Barcelona, Spain; Catalan Institute for Research and Advanced Studies (ICREA), 08003 Barcelona, Spain. Electronic address: acerutti@imim.es.
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  • 2018-10-07
Published in:
  • Immunity. - 2018
B cell
CD44
IgD
Th2
allergy
antibody
basophil
galectin
humoral immunity
mucosal immunity
Animals
Basophils
Cell Line, Tumor
Cells, Cultured
Galectins
Gene Expression Profiling
Humans
Hyaluronan Receptors
Immunoglobulin D
Immunoglobulin E
Immunoglobulin G
Interleukin-4
Mice, Inbred BALB C
Protein Binding
Th2 Cells
English B cells thwart antigenic aggressions by releasing immunoglobulin M (IgM), IgG, IgA, and IgE, which deploy well-understood effector functions. In contrast, the role of secreted IgD remains mysterious. We found that some B cells generated IgD-secreting plasma cells following early exposure to external soluble antigens such as food proteins. Secreted IgD targeted basophils by interacting with the CD44-binding protein galectin-9. When engaged by antigen, basophil-bound IgD increased basophil secretion of interleukin-4 (IL-4), IL-5, and IL-13, which facilitated the generation of T follicular helper type 2 cells expressing IL-4. These germinal center T cells enhanced IgG1 and IgE but not IgG2a and IgG2b responses to the antigen initially recognized by basophil-bound IgD. In addition, IgD ligation by antigen attenuated allergic basophil degranulation induced by IgE co-ligation. Thus, IgD may link B cells with basophils to optimize humoral T helper type 2-mediated immunity against common environmental soluble antigens.
Language
  • English
Open access status
bronze
Identifiers
Persistent URL
https://sonar.ch/global/documents/30462
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