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Turchinovich, G.* ; Vu, T.T.* ; Frommer, F.* ; Kranich, J.* ; Schmid, S.* ; Alles, M.* ; Loubert, J.B.* ; Goulet, J.P.* ; Zimber-Strobl, U. ; Schneider, P.* ; Bachl, J.* ; Pearson, R.* ; Crossley, M.* ; Agenès, F.* ; Kirberg, J.*

Programming of marginal zone B-cell fate by basic Krüppel-like factor (BKLF/KLF3).

Blood 117, 3780-3792 (2011)
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Splenic marginal zone (MZ) B cells are a lineage distinct from follicular and peritoneal B1 B cells. They are located next to the marginal sinus where blood is released. Here they pick up antigens and shuttle the load onto follicular dendritic cells inside the follicle. On activation, MZ B cells rapidly differentiate into plasmablasts secreting antibodies, thereby mediating humoral immune responses against blood-borne type 2 T-independent antigens. As Krüppel-like factors are implicated in cell differentiation/function in various tissues, we studied the function of basic Krüppel-like factor (BKLF/KLF3) in B cells. Whereas B-cell development in the bone marrow of KLF3-transgenic mice was unaffected, MZ B-cell numbers in spleen were increased considerably. As revealed in chimeric mice, this occurred cell autonomously, increasing both MZ and peritoneal B1 B-cell subsets. Comparing KLF3-transgenic and nontransgenic follicular B cells by RNA-microarray revealed that KLF3 regulates a subset of genes that was similarly up-regulated/down-regulated on normal MZ B-cell differentiation. Indeed, KLF3 expression overcame the lack of MZ B cells caused by different genetic alterations, such as CD19-deficiency or blockade of B-cell activating factor-receptor signaling, indicating that KLF3 may complement alternative nuclear factor-κB signaling. Thus, KLF3 is a driving force toward MZ B-cell maturation.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter t-cells; in-vivo; pre-b; lymphocyte-activation; receptor signals; co-repressor; baff; transcription; expression; survival
ISSN (print) / ISBN 0006-4971
e-ISSN 1528-0020
Zeitschrift Blood
Quellenangaben Band: 117, Heft: 14, Seiten: 3780-3792 Artikelnummer: , Supplement: ,
Verlag American Society of Hematology
Verlagsort Washington, USA
Begutachtungsstatus Peer reviewed