{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,24]],"date-time":"2026-03-24T07:08:39Z","timestamp":1774336119177,"version":"3.50.1"},"reference-count":71,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2014,8,1]],"date-time":"2014-08-01T00:00:00Z","timestamp":1406851200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2014,8,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Constitutive expression of Kr\u00fcppel-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 \u03b27 (Itgb7, Ly69) by binding to the \u03b27 promoter, as revealed by chromatin immunoprecipitation. KLF2 overexpression antagonizes this repression and also binds the \u03b27 promoter, indicating that these factors may compete for target sequence(s). Whereas \u03b27 is identified as direct KLF target, its repression by KLF3 is not connected to the MZ B cell increase because \u03b27-deficient mice have a normal complement of these and the KLF3-driven increase still occurs when \u03b27 is deleted. Despite this, KLF3 overexpression abolishes lymphocyte homing to Peyer\u2019s patches, much like \u03b27 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 \u03b27. 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 \u03b27. 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.<\/jats:p>","DOI":"10.4049\/jimmunol.1302613","type":"journal-article","created":{"date-parts":[[2014,7,12]],"date-time":"2014-07-12T03:00:11Z","timestamp":1405134011000},"page":"1737-1746","source":"Crossref","is-referenced-by-count":13,"title":["Leukocyte \u03b27 Integrin Targeted by Kr\u00fcppel-like Factors"],"prefix":"10.1093","volume":"193","author":[{"given":"Melanie","family":"Alles","sequence":"first","affiliation":[{"name":"Division of Immunology (3\/3), Paul-Ehrlich-Institut , 63225 Langen ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gleb","family":"Turchinovich","sequence":"additional","affiliation":[{"name":"Department of Biomedicine, Laboratory of Developmental Immunology , 4058 Basel ,","place":["Switzerland"]},{"name":"Basel University Children's Hospital , 4031 Basel ,","place":["Switzerland"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Pumin","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Molecular Physiology and Biophysics, Baylor College of Medicine , Houston, TX 77030"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wolfgang","family":"Schuh","sequence":"additional","affiliation":[{"name":"Division of Molecular Immunology, Department of Internal Medicine III, Nikolaus-Fiebiger-Center, University of Erlangen-N\u00fcrnberg , 91054 Erlangen ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fabien","family":"Agen\u00e8s","sequence":"additional","affiliation":[{"name":"INSERM U743 , Montreal, Quebec H2X 1P1 ,","place":["Canada"]},{"name":"INSERM ADR Paris V Saint Anne , 75014 Paris ,","place":["France"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J\u00f6rg","family":"Kirberg","sequence":"additional","affiliation":[{"name":"Division of Immunology (3\/3), Paul-Ehrlich-Institut , 63225 Langen ,","place":["Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2014,8,15]]},"reference":[{"key":"2025030707281420600_r1","doi-asserted-by":"crossref","first-page":"474","DOI":"10.1016\/j.ygeno.2005.12.011","article-title":"Human KLF17 is a new member of the Sp\/KLF family of transcription factors","volume":"87","author":"van Vliet","year":"2006","journal-title":"Genomics"},{"key":"2025030707281420600_r2","doi-asserted-by":"crossref","first-page":"241","DOI":"10.1016\/j.tcm.2004.06.005","article-title":"An emerging role for Kr\u00fcppel-like factors in vascular biology","volume":"14","author":"Feinberg","year":"2004","journal-title":"Trends Cardiovasc. 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