{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T14:32:21Z","timestamp":1793370741242,"version":"4.5.0"},"reference-count":36,"publisher":"National Academy of Sciences","issue":"2","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2011,1,11]]},"abstract":"<jats:p>\n                    The transcription factor Kr\u00fcppel-like factor 2 (KLF2) is critical for normal trafficking of T lymphocytes, but its role in B cells is unclear. We report that B cell-specific KLF2 deficiency leads to decreased expression of the trafficking molecules CD62L and \u03b27-integrin, yet expression of sphingosine-1 phosphate receptor 1 (which is a critical target of KLF2 in T cells) was, unexpectedly, minimally altered. Unexpectedly,\n                    <jats:italic>Klf2<\/jats:italic>\n                    deletion led to a drastic reduction in the B1 B-cell pool and a substantial increase in transitional and marginal zone B-cell numbers. In addition, we observed that KLF2-deficient B cells showed increased apoptosis and impaired proliferation after B-cell receptor cross-linking. Gene expression analysis indicated that KLF2-deficient follicular B cells display numerous characteristics shared by normal marginal zone B cells, including reduced expression of several signaling molecules that may contribute to defective activation of these cells. Hence, our data indicate that KLF2 plays a critical role in dictating normal subset differentiation and functional reactivity of mature B cells.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1013168108","type":"journal-article","created":{"date-parts":[[2010,12,27]],"date-time":"2010-12-27T20:45:14Z","timestamp":1293482714000},"page":"716-721","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":120,"title":["Kr\u00fcppel-like factor 2 (KLF2) regulates B-cell reactivity, subset differentiation, and trafficking molecule expression"],"prefix":"10.1073","volume":"108","author":[{"given":"Geoffrey T.","family":"Hart","sequence":"first","affiliation":[{"name":"Department of Laboratory Medicine and Pathology, Center for Immunology, University of Minnesota, Minneapolis, MN 55414"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaodan","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine and Pathology, Center for Immunology, University of Minnesota, Minneapolis, MN 55414"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kristin A.","family":"Hogquist","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine and Pathology, Center for Immunology, University of Minnesota, Minneapolis, MN 55414"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen C.","family":"Jameson","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine and Pathology, Center for Immunology, University of Minnesota, Minneapolis, MN 55414"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2010,12,27]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.biocel.2007.07.018"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature04882"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.178.12.7632"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2009.05.011"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1207996"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/90633"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.277.5334.1986"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.molimm.2007.06.154"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1034\/j.1600-065X.2000.00614.x"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature02284"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/1074-7613(94)90076-0"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.coi.2008.03.014"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1038\/nri955"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.0105-2896.2003.097.x"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.177.5.2749"},{"key":"e_1_3_3_16_2","doi-asserted-by":"publisher","DOI":"10.1038\/35105052"},{"key":"e_1_3_3_17_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2007.05.013"},{"key":"e_1_3_3_18_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20051038"},{"key":"e_1_3_3_19_2","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/25.6.1317"},{"key":"e_1_3_3_20_2","doi-asserted-by":"publisher","DOI":"10.1038\/ni1083"},{"key":"e_1_3_3_21_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20041509"},{"key":"e_1_3_3_22_2","doi-asserted-by":"crossref","first-page":"4371","DOI":"10.4049\/jimmunol.157.10.4371","article-title":"CD19 regulates B lymphocyte signaling thresholds critical for the development of B-1 lineage cells and autoimmunity","volume":"157","author":"Sato S","year":"1996","unstructured":"S Sato, N Ono, DA Steeber, DS Pisetsky, TF Tedder, CD19 regulates B lymphocyte signaling thresholds critical for the development of B-1 lineage cells and autoimmunity. 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