NDLI: Leukocyte ß7 integrin targeted by Krüppel-like factors.

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Leukocyte ß7 integrin targeted by Krüppel-like factors.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Alles, Melanie Schuh, Wolfgang Kirberg, Jörg Zhang, Pumin Agenès, Fabien Turchinovich, Gleb
Description	Author Affiliation: Alles M ( Division of Immunology (3/3), Paul-Ehrlich-Institut, 63225 Langen, Germany); Turchinovich G ( Department of Biomedicine, Laboratory of Developmental Immunology, 4058 Basel, Switzerland); Zhang P ( Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX 77030); Schuh W ( Division of Molecular Immunology, Department of Internal Medicine III, Nikolaus-Fiebiger-Center, University of Erlangen-Nürnberg, 91054 Erlangen, Germany); Agenès F ( INSERM U743, Montreal, Quebec H2X 1P1, Canada); Kirberg J ( Division of Immunology (3/3), Paul-Ehrlich-Institut, 63225 Langen, Germany)
Abstract	Constitutive expression of Krüppel-like factor 3 (KLF3, BKLF) increases marginal zone (MZ) B cell numbers, a phenotype shared with mice lacking KLF2. Ablation of KLF3, known to interact with serum response factor (SRF), or SRF itself, results in fewer MZ B cells. It is unknown how these functional equivalences result. In this study, it is shown that KLF3 acts as transcriptional repressor for the leukocyte-specific integrin ß7 (Itgb7, Ly69) by binding to the ß7 promoter, as revealed by chromatin immunoprecipitation. KLF2 overexpression antagonizes this repression and also binds the ß7 promoter, indicating that these factors may compete for target sequence(s). Whereas ß7 is identified as direct KLF target, its repression by KLF3 is not connected to the MZ B cell increase because ß7-deficient mice have a normal complement of these and the KLF3-driven increase still occurs when ß7 is deleted. Despite this, KLF3 overexpression abolishes lymphocyte homing to Peyer's patches, much like ß7 deficiency does. Furthermore, KLF3 expression alone overcomes the MZ B cell deficiency when SRF is absent. SRF is also dispensable for the KLF3-mediated repression of ß7. Thus, despite the shared phenotype of KLF3 and SRF-deficient mice, cooperation of these factors appears neither relevant for the formation of MZ B cells nor for the regulation of ß7. Finally, a potent negative regulatory feedback loop limiting KLF3 expression is shown in this study, mediated by KLF3 directly repressing its own gene promoter. In summary, KLFs use regulatory circuits to steer lymphocyte maturation and homing and directly control leukocyte integrin expression.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	4
Volume Number	193
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-08-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	B-lymphocytes Immunology Integrin Beta Chains Genetics Kruppel-like Transcription Factors Lymphopoiesis Animals Antigens, Cd11 Biosynthesis Cell Differentiation Cells, Cultured Dna-binding Proteins Gene Expression Regulation Integrin Alpha Chains Mice Mice, Inbred C57bl Mice, Transgenic Peyer's Patches Promoter Regions, Genetic Protein Binding Serum Response Factor Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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