biostudies-literatureGlinton KNCATS NIH HHSNIAID NIH HHSNHLBI NIH HHSNational Institutes of Health435-446https://www.ebi.ac.uk/biostudies/studies/S-EPMC8169599biostudies-literatureUnknown40(6)Cardiac Allograft Vasculopathy (CAV) is a leading contributor to late transplant rejection. Although implicated, the mechanisms by which bone marrow-derived cells promote CAV remain unclear. Emerging evidence implicates the cell surface receptor tyrosine kinase AXL to be elevated in rejecting human allografts. AXL protein is found on multiple cell types, including bone marrow-derived myeloid cells. The causal role of AXL from this compartment and during transplant is largely unknown. This is important because AXL is a key regulator of myeloid inflammation. Utilizing experimental chimeras deficient in the bone marrow-derived Axl gene, we report that Axl antagonizes cardiac allograft survival and promotes CAV. Flow cytometric and histologic analyses of Axl-deficient transplant recipients revThe Journal of heart and lung transplantation : the official publication of the International Society for Heart TransplantationBone marrow-derived AXL tyrosine kinase promotes mitogenic crosstalk and cardiac allograft vasculopathy.PMC8169599UL1 TR001422R01 HL122309R01 HL139812R01 AI114824Ansari MJLomasney JSinha ALeventhal JRFeinstein MGlinton KThorp EBFisher EWasserstrom JAZhang ZJDeBerge MSchroth SForbess JMLuo XWang JJfalseBone marrow-derived AXL tyrosine kinase promotes mitogenic crosstalk and cardiac allograft vasculopathy.Cardiac Allograft Vasculopathy (CAV) is a leading contributor to late transplant rejection. Although implicated, the mechanisms by which bone marrow-derived cells promote CAV remain unclear. Emerging evidence implicates the cell surface receptor tyrosine kinase AXL to be elevated in rejecting human allografts. AXL protein is found on multiple cell types, including bone marrow-derived myeloid cells. The causal role of AXL from this compartment and during transplant is largely unknown. This is important because AXL is a key regulator of myeloid inflammation. Utilizing experimental chimeras deficient in the bone marrow-derived Axl gene, we report that Axl antagonizes cardiac allograft survival and promotes CAV. Flow cytometric and histologic analyses of Axl-deficient transplant recipients rev2021-01-01T00:00:00Z2021 Jun2025-04-22T21:54:55.234Z2025-04-06T03:52:10.181ZS-EPMC81695993384607910.1016/j.healun.2021.03.006