Deletion of IL-4Rα signaling on B cells limits hyperresponsiveness depending on antigen load

J Allergy Clin Immunol. 2021 Jul;148(1):99-109.e5. doi: 10.1016/j.jaci.2020.12.635. Epub 2020 Dec 28.

Abstract

Background: B cells play an important role in allergies through secretion of IgE. IL-4 receptor α (IL-4Rα) is key in allergic asthma and regulates type 2 cytokine production, IgE secretion, and airway hyperresponsiveness. IL-4 activation of B cells is essential for class switching and contributes to the induction of B effector 2 (Be2) cells. The role of Be2 cells and signaling via IL-4Rα in B cells is not clearly defined.

Objective: We sought to find out whether IL-4Rα-responsive B cells or Be2 function was essential in experimental allergic asthma.

Methods: Mice lacking IL-4Rα on B cells (mb1creIL-4Rα-/lox) or littermate controls (IL-4Rα-/lox) and mice lacking IL-4 or IL-4/IL-13 on B cells were sensitized and challenged with high-dose house dust mite (>10 μg) or with low-dose house dust mite (<3 μg). We also adoptively transferred naive IL-4Rα-/lox or IL-4Rα-/- B cells into μMT-/- mice a day before sensitization or a day before challenge. We analyzed lung inflammation, cellular infiltrate, and airway hyperresponsiveness.

Results: We found that IL-4Rα signaling on B cells was important for optimal TH2 allergic immune responses mainly when the load of antigen is limited. IL-4Rα signaling on B cells was essential for germinal centers and in the effector phase of allergic responses. Be2 cells were essential in airway hyperresponsiveness, but not in other parameters.

Conclusions: IL-4Rα signaling on B cells is deleterious in allergic asthma because it is required for optimal TH2 responses, Be2 function, germinal center formation, and T follicular helper cells, especially when the load of the antigen is limiting.

Keywords: B cells; B effector 2 cells; IL-4Rα; T follicular helper cell; T(H)2 cells; germinal center.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Allergens / immunology
  • Animals
  • Antigens / immunology*
  • Asthma / immunology
  • B-Lymphocytes / immunology*
  • Hypersensitivity / immunology*
  • Interleukin-13 / immunology
  • Interleukin-4 Receptor alpha Subunit / immunology*
  • Lung / immunology
  • Mice
  • Mice, Inbred BALB C
  • Pneumonia / immunology
  • Pyroglyphidae / immunology
  • Respiratory Hypersensitivity / immunology*
  • Signal Transduction / immunology*
  • Th2 Cells / immunology

Substances

  • Allergens
  • Antigens
  • Interleukin-13
  • Interleukin-4 Receptor alpha Subunit