biostudies-literatureBatchu NNIAID NIH HHSNHLBI NIH HHS1638-1646https://www.ebi.ac.uk/biostudies/studies/S-EPMC5096552biostudies-literatureUnknown36(8)<h4>Objective</h4>Survival of immune and nonimmune cells relies on Axl, a receptor tyrosine kinase, which is implicated in hypertension. Activated T lymphocytes are involved in regulation of high blood pressure. The goal of the study was to investigate the role of Axl in T-lymphocyte functions and its contribution to salt-dependent hypertension.<h4>Approach and results</h4>We report increased apoptosis in peripheral blood from Axl(-/-) mice because of lower numbers of white blood cells mostly lymphocytes. In vitro studies showed modest reduction in interferon gamma production in Axl(-/-) type 1 T helper cells. Axl did not affect basic proliferation capacity or production of interleukin 4 in Axl(-/-) type 2 T helper cells. However, competitive repopulation of Axl(-/-) bone marrow or adoptive transfer of Axl(-/-) CD4(+) T cells to Rag1(-/-) mice showed robust effect of Axl on T lymphocyte expansion in vivo. Adoptive transfer of Axl(-/-) CD4(+) T cells was protective in a later phase of deoxycorticosterone-acetate and salt hypertension. Reduced numbers of CD4(+) T cells in circulation and in perivascular adventitia decreased vascular remodeling and increased vascular apoptosis in the late phase of hypertension.<h4>Conclusions</h4>These findings suggest that Axl is critical for survival of T lymphocytes, especially during vascular remodeling in hypertension.Arteriosclerosis, thrombosis, and vascular biologyRole of Axl in T-Lymphocyte Survival in Salt-Dependent Hypertension.PMC5096552P01 AI102851R01 AI072690R01 HL105623R01 HL124018Wadosky KMMorrell CNFowell DJBatchu NKorshunov VAHughson AfalseRole of Axl in T-Lymphocyte Survival in Salt-Dependent Hypertension.<h4>Objective</h4>Survival of immune and nonimmune cells relies on Axl, a receptor tyrosine kinase, which is implicated in hypertension. Activated T lymphocytes are involved in regulation of high blood pressure. The goal of the study was to investigate the role of Axl in T-lymphocyte functions and its contribution to salt-dependent hypertension.<h4>Approach and results</h4>We report increased apoptosis in peripheral blood from Axl(-/-) mice because of lower numbers of white blood cells mostly lymphocytes. In vitro studies showed modest reduction in interferon gamma production in Axl(-/-) type 1 T helper cells. Axl did not affect basic proliferation capacity or production of interleukin 4 in Axl(-/-) type 2 T helper cells. However, competitive repopulation of Axl(-/-) bone marrow or adoptive transfer of Axl(-/-) CD4(+) T cells to Rag1(-/-) mice showed robust effect of Axl on T lymphocyte expansion in vivo. Adoptive transfer of Axl(-/-) CD4(+) T cells was protective in a later phase of deoxycorticosterone-acetate and salt hypertension. Reduced numbers of CD4(+) T cells in circulation and in perivascular adventitia decreased vascular remodeling and increased vascular apoptosis in the late phase of hypertension.<h4>Conclusions</h4>These findings suggest that Axl is critical for survival of T lymphocytes, especially during vascular remodeling in hypertension.2016-01-01T00:00:00Z2016 Aug2025-04-18T20:50:10.403Z2019-03-27T02:28:17ZS-EPMC50965522736540410.1161/ATVBAHA.116.30784810.1161/atvbaha.116.307848