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Hoogenboezem, M.

Publications and source records attributed to Hoogenboezem, M..

3 recordsLinked to original sources

Leukocytes use endothelial membrane tunnels to extravasate the vasculature

Upon inflammation, leukocytes extravasate through endothelial cells. When they extravasate in a paracellular manner, it is generally accepted that neighbouring endothelial cells physically disconnect to open cell-cell junctions, allowing leukocytes to cross. When carefully examining endothelial junctions, we found a partial membrane overlap of endothelial cells beyond VE-cadherin distribution. These overlaps are regulated by actin polymerization and, although marked by, do not require PECAM-1, nor VE-cadherin. Neutrophils prefer wider membrane overlaps as exit sites. Detailed 3D analysis of endothelial membrane dynamics during paracellular neutrophil transmigration in real-time, at high spatiotemporal resolution using resonant confocal and lattice light-sheet imaging, revealed that overlapping endothelial membranes form a tunnel during neutrophil transmigration. These tunnels are formed by the neutrophil lifting the membrane of the upper endothelial cell while indenting and crawling over the membrane of the underlying endothelial cell. Our work shows that endothelial cells do not simply retract upon passage of neutrophils but provide membrane tunnels, allowing neutrophils to extravasate. This discovery defines the 3D multicellular architecture in which the paracellular transmigration of neutrophils occurs.

cell biology↗

SIRPalpha on mouse B1 cells restricts lymphoid tissue migration and natural antibody production

The inhibitory immunoreceptor SIRP is expressed on myeloid and neuronal cells and interacts with the broadly expressed CD47. CD47-SIRP interactions form an innate immune checkpoint and its targeting has shown promising results in cancer patients. Here, we report expression of SIRP on B1 lymphocytes, a non-conventional subpopulation of murine B cells responsible for the production of natural antibodies. Mice defective in SIRP signaling (SIRP{Delta}CYT mice) displayed an enhanced CD11b/CD18 integrin-dependent B1 cell migration from the peritoneal cavity to the spleen, local B1 cell accumulation, and enhanced circulating natural antibody levels, which was further amplified upon immunization with T-independent type 2 antigen. As natural antibodies are atheroprotective we investigated the involvement of SIRP signaling in atherosclerosis development. Bone marrow (SIRP{Delta}CYT>LDLR-/-) chimaeric mice developed reduced atherosclerosis accompanied by increased natural antibody production. Collectively, our data identify SIRP as a unique B1 cell inhibitory receptor acting to control B1 cell migration, and imply SIRP as a potential therapeutic target in atherosclerosis.

immunology↗

Hematopoietic Stem And Progenitor Cells Use Podosomes To Transcellularly Home To The Bone Marrow.

Bone marrow (BM) endothelium plays an important role in homing of hematopoietic stem and progenitor cells (HSPCs) upon transplantation, but surprisingly little is known on how endothelial cells regulate local permeability and HSPC transmigration. We show that temporal loss of VE-cadherin function promotes vascular permeability in BM, even upon low dose irradiation and strongly enhanced homing of transplanted HSPCs to BM of irradiated mice. Intriguingly, stabilizing junctional VE-cadherin in vivo reduced BM permeability, but did not prevent HSPC migration into the BM, suggesting that HSPCs enter the bone marrow by transcellularly crossing the endothelium. Indeed, HSPCs induce podosomes to cross human BM endothelial monolayers in a transcellular manner. By contrast, HSPC rather use the paracellular route when VE-cadherin function is inhibited. Taken together, VE-cadherin is crucial for BM vascular homeostasis and HSPC homing, and may therefore serve as a potential therapeutic target to improve HSPC homing strategies.

cell biology↗