<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Day CE</submitter><funding>Wellcome Trust</funding><pagination>564-71</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2913267</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>130(4)</volume><pubmed_abstract>The ability of T cells to microlocalize within tissues, such as the lung, is crucial for immune surveillance and increased T-cell infiltration is a feature of many inflammatory lung conditions. T-cell migration has mainly been studied in two-dimensional assays. Using three-dimensional collagen gels to mimic the extracellular matrix of lung tissue, we have characterized the migration of T lymphocytes isolated from peripheral blood (PBT) and lung (LT) in response to interleukin-2 (IL-2) and CXCL12. Freshly isolated PBT and LT showed a low degree of migration (blood 4.0 +/- 1.3% and lung 4.1 +/- 1.7%). Twenty-four hours of culture increased the percentage of migrating PBT and LT (blood 17.5 +/- 2.9% and lung 17.7 +/- 3.8%). The IL-2 stimulation modestly increased migration of PBT after 6 days (32.3 +/- 6.0%), but had no effect on the migration of LT (25.5 +/- 3.2%). Twenty-four hours of stimulation with anti-CD3/CD28 caused a small but significant increase in the migration of PBT (to 36.4 +/- 5.8%). In a directional three-dimensional assay, CXCL12 failed to induce migration of fresh PBT or LT. Twenty-four hours of culture, which increased CXCR4 expression of PBT 3.6-fold, significantly increased the migration of PBT in response to CXCL12. Migration of PBT to CXCL12 was blocked by pertussis toxin, but not by the phosphoinositide 3-kinase inhibitor wortmannin. Twenty-four-hour cultured LT did not respond to CXCL12. CD3/CD28-stimulation inhibited CXCL12-mediated migration of PBT. These results suggest that the migration pattern of PBT is distinct from that of LT.</pubmed_abstract><journal>Immunology</journal><pubmed_title>Characterization of the migration of lung and blood T cells in response CXCL12 in a three-dimensional matrix.</pubmed_title><pmcid>PMC2913267</pmcid><funding_grant_id>073983</funding_grant_id><pubmed_authors>Day CE</pubmed_authors><pubmed_authors>Wardlaw AJ</pubmed_authors><pubmed_authors>Willars GB</pubmed_authors><pubmed_authors>Guillen C</pubmed_authors></additional><is_claimable>false</is_claimable><name>Characterization of the migration of lung and blood T cells in response CXCL12 in a three-dimensional matrix.</name><description>The ability of T cells to microlocalize within tissues, such as the lung, is crucial for immune surveillance and increased T-cell infiltration is a feature of many inflammatory lung conditions. T-cell migration has mainly been studied in two-dimensional assays. Using three-dimensional collagen gels to mimic the extracellular matrix of lung tissue, we have characterized the migration of T lymphocytes isolated from peripheral blood (PBT) and lung (LT) in response to interleukin-2 (IL-2) and CXCL12. Freshly isolated PBT and LT showed a low degree of migration (blood 4.0 +/- 1.3% and lung 4.1 +/- 1.7%). Twenty-four hours of culture increased the percentage of migrating PBT and LT (blood 17.5 +/- 2.9% and lung 17.7 +/- 3.8%). The IL-2 stimulation modestly increased migration of PBT after 6 days (32.3 +/- 6.0%), but had no effect on the migration of LT (25.5 +/- 3.2%). Twenty-four hours of stimulation with anti-CD3/CD28 caused a small but significant increase in the migration of PBT (to 36.4 +/- 5.8%). In a directional three-dimensional assay, CXCL12 failed to induce migration of fresh PBT or LT. Twenty-four hours of culture, which increased CXCR4 expression of PBT 3.6-fold, significantly increased the migration of PBT in response to CXCL12. Migration of PBT to CXCL12 was blocked by pertussis toxin, but not by the phosphoinositide 3-kinase inhibitor wortmannin. Twenty-four-hour cultured LT did not respond to CXCL12. CD3/CD28-stimulation inhibited CXCL12-mediated migration of PBT. These results suggest that the migration pattern of PBT is distinct from that of LT.</description><dates><release>2010-01-01T00:00:00Z</release><publication>2010 Aug</publication><modification>2025-04-26T21:02:52.509Z</modification><creation>2019-03-27T00:32:52Z</creation></dates><accession>S-EPMC2913267</accession><cross_references><pubmed>20331475</pubmed><doi>10.1111/j.1365-2567.2010.03257.x</doi></cross_references></HashMap>