{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T05:45:26Z","timestamp":1770097526200,"version":"3.49.0"},"reference-count":44,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2005,11,1]],"date-time":"2005-11-01T00:00:00Z","timestamp":1130803200000},"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":[[2005,11,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>T cells deficient in the Tec kinases Itk or Itk and Rlk exhibit defective TCR-stimulated proliferation, IL-2 production, and activation of phospholipase C-\u03b3. Evidence also implicates Tec kinases in actin cytoskeleton regulation, which is necessary for cell adhesion and formation of the immune synapse in T lymphocytes. In this study we show that Tec kinases are required for TCR-mediated up-regulation of adhesion via the LFA-1 integrin. We also demonstrate that the defect in adhesion is associated with defective clustering of LFA-1 and talin at the site of interaction of Rlk\u2212\/\u2212Itk\u2212\/\u2212 and Itk\u2212\/\u2212 T cells with anti-TCR-coated beads. Defective recruitment of Vav1, protein kinase C\u03b8, and Pyk2 was also observed in Rlk\u2212\/\u2212Itk\u2212\/\u2212 and Itk\u2212\/\u2212 T cells. Stimulation with ICAM-2 in conjunction with anti-TCR-coated beads enhanced polarization of Vav1, protein kinase C\u03b8, and Pyk2 in wild-type cells, demonstrating a role for integrins in potentiating the recruitment of signaling molecules in T cells. Increased recruitment of signaling molecules was most pronounced under conditions of low TCR stimulation. Under these suboptimal TCR stimulation conditions, ICAM-2 could also enhance the recruitment of signaling molecules in Itk\u2212\/\u2212, but not Rlk\u2212\/\u2212Itk\u2212\/\u2212 T cells. Thus, Tec kinases play key roles in regulating TCR-mediated polarization of integrins and signaling molecules to the site of TCR stimulation as well as the up-regulation of integrin adhesion.<\/jats:p>","DOI":"10.4049\/jimmunol.175.9.5923","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T22:54:18Z","timestamp":1398034458000},"page":"5923-5930","source":"Crossref","is-referenced-by-count":36,"title":["Tec Kinases Regulate TCR-Mediated Recruitment of Signaling Molecules and Integrin-Dependent Cell Adhesion"],"prefix":"10.1093","volume":"175","author":[{"given":"Lisa D","family":"Finkelstein","sequence":"first","affiliation":[{"name":"National Human Genome Research Institute, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yoji","family":"Shimizu","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine and Pathology, Center for Immunology, and Cancer Center University of Minnesota , Minneapolis, MN 55455"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Pamela L","family":"Schwartzberg","sequence":"additional","affiliation":[{"name":"National Human Genome Research Institute, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2005,11,1]]},"reference":[{"key":"2026020212143179100_R1","first-page":"100","volume-title":"Immunol. 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