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Journal Article

Integrin β1 regulates marginal zone B cell differentiation and PI3K signaling

MPS-Authors

Andreani,  Virginia
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Ramamoorthy,  Senthilkumar
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Grosschedl,  Rudolf
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

External Resource

https://rupress.org/jem/article/220/1/e20220342/213672/Integrin-1-regulates-marginal-zone-B-cell
(Publisher version)

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Fulltext (public)

10.1084_jem.20220342.pdf
(Publisher version), 9MB

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Citation

Andreani, V., Ramamoorthy, S., Fässler, R., & Grosschedl, R. (2022). Integrin β1 regulates marginal zone B cell differentiation and PI3K signaling. Journal of Experimental Medicine, 220: e20220342. doi:10.1084/jem.20220342.


Cite as: https://hdl.handle.net/21.11116/0000-000C-2B2E-2
Abstract
Marginal zone (MZ) B cells represent innate-like B cells that mediate a fast immune response. The adhesion of MZ B cells to the marginal sinus of the spleen is governed by integrins. Here, we address the question of whether β1-integrin has additional functions by analyzing Itgb1fl/flCD21Cre mice in which the β1-integrin gene is deleted in mature B cells. We find that integrin β1–deficient mice have a defect in the differentiation of MZ B cells and plasma cells. We show that integrin β1–deficient transitional B cells, representing the precursors of MZ B cells, have enhanced B cell receptor (BCR) signaling, altered PI3K and Ras/ERK pathways, and an enhanced interaction of integrin-linked kinase (ILK) with the adaptor protein Grb2. Moreover, the MZ B cell defect of integrin β1–deficient mice could, at least in part, be restored by a pharmacological inhibition of the PI3K pathway. Thus, β1-integrin has an unexpected function in the differentiation and function of MZ B cells.