Print Email Facebook Twitter Natural killer cells and CD4+ T-cells modulate collateral artery development Title Natural killer cells and CD4+ T-cells modulate collateral artery development Author van Weel, V. Toes, R.E.M. Seghers, L. Deckers, M.M.L. de Vries, M.R. Eilers, P.H. Sipkens, J. Schepers, A. Eefting, D. van Hinsbergh, V.W.M. van Bockel, J.H. Quax, P.H.A. TNO Kwaliteit van Leven Publication year 2007 Abstract OBJECTIVE - The immune system is thought to play a crucial role in regulating collateral circulation (arteriogenesis), a vital compensatory mechanism in patients with arterial obstructive disease. Here, we studied the role of lymphocytes in a murine model of hindlimb ischemia. METHODS AND RESULTS - Lymphocytes, detected with markers for NK1.1, CD3, and CD4, invaded the collateral vessel wall. Arteriogenesis was impaired in C57BL/6 mice depleted for Natural Killer (NK)-cells by anti-NK1.1 antibodies and in NK-cell-deficient transgenic mice. Arteriogenesis was, however, unaffected in Jα281-knockout mice that lack NK1.1 Natural Killer T (NKT)-cells, indicating that NK-cells, rather than NKT-cells, are involved in arteriogenesis. Furthermore, arteriogenesis was impaired in C57BL/6 mice depleted for CD4 T-lymphocytes by anti-CD4 antibodies, and in major histocompatibility complex (MHC)-class-II-deficient mice that more selectively lack mature peripheral CD4 T-lymphocytes. This impairment was even more profound in anti-NK1.1-treated MHC-class-II-deficient mice that lack both NK- and CD4 T-lymphocytes. Finally, collateral growth was severely reduced in BALB/c as compared with C57BL/6 mice, 2 strains with different bias in immune responsiveness. CONCLUSIONS - These data show that both NK-cells and CD4 T-cells modulate arteriogenesis. Promoting lymphocyte activation may represent a promising method to treat ischemic disease. © 2007 American Heart Association, Inc. Subject Biomedical ResearchAngiogenesisAnimal models of human diseasePeripheral vascular diseasebiological markerCD3 antigenCD4 antigenvascularizationAnimalsArterial Occlusive DiseasesCD4-Positive T-LymphocytesCollateral CirculationDisease Models, AnimalFemoral ArteryHindlimbIschemiaKiller Cells, NaturalMiceMice, Inbred BALB CMice, KnockoutNeovascularization, Physiologic To reference this document use: http://resolver.tudelft.nl/uuid:5dcb7cad-19a2-436b-8a7a-a444480e4f5d DOI https://doi.org/10.1161/atvbaha.107.151407 TNO identifier 240272 ISSN 1079-5642 Source Arteriosclerosis, Thrombosis, and Vascular Biology, 27 (11), 2310-2318 Document type article Files To receive the publication files, please send an e-mail request to TNO Library.