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. 2023 May 12;14:1172641. doi: 10.3389/fimmu.2023.1172641

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Copyright © 2023 Wittner and Schuh

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Krüppel-like factor-2 (KLF2) contributes to the termination of pre-B cell expansion through inhibition of Jun/Fos and Egr1/2. Moreover, KLF2 inhibits the proliferation of pre-B cells and the activation of naïve, mature B cells by downregulating c-myc and upregulating p21 and p27. In B cells, KLF2 suppresses NF-κB activation. Furthermore, KLF2 represses Notch2 signaling in naïve B cells, thereby driving B cell differentiation to follicular B cells. KLF2 controls the migration of B cells and plasmablasts by positively regulating L-Selectin, Itgα4β7, Itgα4β1, ItgαM, Chemokine receptor 9 (CCR9), Sphingosine-1-Phosphate-Receptor (S1PR) 1 and S1PR4. IgA plasmablast homing to gut-associated lymphoid tissues (GALT) is mediated by KLF2-regulated factors Itgα4β7 and CCR9. Itg, integrin.