Abstract
Abstract CXCL13 is a homeostatic chemokine instrumental in guided lymphocyte and dendritic cell trafficking towards lymphoid organs and stromal tissue. Evidence is culminating that in various chronic immune disorders extranodal CXCL13 expression at the site of inflammation contributes to the disease. Here we addressed the role of CXCL13 and its receptor CXCR5 in atherosclerosis. Bone marrow ablated LDLr-/- mice were repopulated with CXCL13 KO and CXCR5 KO bone marrow cells and after recovery fed a high-fat diet for 14 weeks. Carotid artery lesions were induced by perivascular collar placement. Both CXCL13 and CXCR5 deficiency resulted in significant attenuation of atherosclerosis, characterized by a decreased infiltration of granulocytes into the lesions. Haematopoietic deficiency of CXCR5 resulted in impaired homing of B cells and regulatory T cells towards peripheral lymph nodes. However, we didn’t observe this effect in the CXCL13 KO group. Surprisingly, FACS analysis showed a significant reduction in circulating CD11b+Ly6C+ pro-inflammatory monocytes and granulocytes both in the CXCR5 KO and CXCL13 KO group. In addition, plasma levels of M-CSF, G-CSF and RANK-L were strongly reduced. To conclude, haematopoietic deficiency of CXCL13/CXCR5 attenuates atherogenesis, probably attributable to the effects seen on Ly6Chighmonocyte and granulocyte levels in circulation. This study is the first to describe a critical role for the CXCL13/CXCR5 axis in myeloid development.
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