Group 2 innate lymphoid cells are a non-redundant source of interleukin-5 required for development and function of murine B1 cells

Karoline F. Troch, Manuel O. Jakob, Patrycja M. Forster, Katja J. Jarick, Jonathan Schreiber, Alexandra Preusser, Gabriela M. Guerra, Pawel Durek, Caroline Tizian, Nele Sterczyk, Sofia Helfrich, Claudia U. Duerr, David Voehringer, Mario Witkowski, David Artis, Tim Rollenske, Andrey A. Kruglov, Mir-Farzin Mashreghi and Christoph S. N. Klose ()
Additional contact information
Karoline F. Troch: Corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Microbiology, Infectious Diseases and Immunology, Hindenburgdamm 30
Manuel O. Jakob: Corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Microbiology, Infectious Diseases and Immunology, Hindenburgdamm 30
Patrycja M. Forster: Corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Microbiology, Infectious Diseases and Immunology, Hindenburgdamm 30
Katja J. Jarick: Corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Microbiology, Infectious Diseases and Immunology, Hindenburgdamm 30
Jonathan Schreiber: University Hospital Bonn
Alexandra Preusser: Corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Microbiology, Infectious Diseases and Immunology, Hindenburgdamm 30
Gabriela M. Guerra: an Institute of the Leibniz Association
Pawel Durek: an Institute of the Leibniz Association
Caroline Tizian: Corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Microbiology, Infectious Diseases and Immunology, Hindenburgdamm 30
Nele Sterczyk: Corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Microbiology, Infectious Diseases and Immunology, Hindenburgdamm 30
Sofia Helfrich: Corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Microbiology, Infectious Diseases and Immunology, Hindenburgdamm 30
Claudia U. Duerr: Corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Microbiology, Infectious Diseases and Immunology, Hindenburgdamm 30
David Voehringer: Friedrich-Alexander University Erlangen-Nuremberg
Mario Witkowski: Corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Microbiology, Infectious Diseases and Immunology, Hindenburgdamm 30
David Artis: Cornell University
Tim Rollenske: University Hospital Bonn
Andrey A. Kruglov: an Institute of the Leibniz Association
Mir-Farzin Mashreghi: an Institute of the Leibniz Association
Christoph S. N. Klose: Corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Microbiology, Infectious Diseases and Immunology, Hindenburgdamm 30

Nature Communications, 2024, vol. 15, issue 1, 1-12

Abstract: Abstract Tissue-resident immune cells, such as innate lymphoid cells, mediate protective or detrimental immune responses at barrier surfaces. Upon activation by stromal or epithelial cell-derived alarmins, group 2 innate lymphoid cells (ILC2s) are a rapid source of type 2 cytokines, such as IL-5. However, due to the overlap in effector functions, it remains unresolved whether ILC2s are an essential component of the type 2 response or whether their function can be compensated by other cells, such as T cells. Here we show a non-redundant role of ILC2s in supporting the development and function of B1 cells. We demonstrate that B1 cells fail to develop properly in the absence of ILC2s and identify the IL-33 receptor on ILC2s as an essential cell-intrinsic regulator of IL-5 production. Further, conditional deletion of Il5 in ILC2s results in defective B1 cell development and immunoglobulin production. Consequently, B1 cells with phosphatidylcholine specific B cell receptor rearrangements are diminished in ILC2-deficient mice. Thus, our data establish an essential function of ILC2s in supporting B1 cells and antibody production at barrier surfaces.

Date: 2024
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DOI: 10.1038/s41467-024-54780-3

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