@article{18109,
  abstract     = {Venous thromboembolism (VTE) is a common, deadly disease with an increasing incidence despite preventive efforts. Clinical observations have associated elevated antibody concentrations or antibody-based therapies with thrombotic events. However, how antibodies contribute to thrombosis is unknown. Here, we show that reduced blood flow enabled immunoglobulin M (IgM) to bind to FcμR and the polymeric immunoglobulin receptor (pIgR), initiating endothelial activation and platelet recruitment. Subsequently, the procoagulant surface of activated platelets accommodated antigen- and FcγR-independent IgG deposition. This leads to classical complement activation, setting in motion a prothrombotic vicious circle. Key elements of this mechanism were present in humans in the setting of venous stasis as well as in the dysregulated immunothrombosis of COVID-19. This antibody-driven thrombosis can be prevented by pharmacologically targeting complement. Hence, our results uncover antibodies as previously unrecognized central regulators of thrombosis. These findings carry relevance for therapeutic application of antibodies and open innovative avenues to target thrombosis without compromising hemostasis.},
  author       = {Stark, Konstantin and Kilani, Badr and Stockhausen, Sven and Busse, Johanna and Schubert, Irene and Tran, Thuy Duong and Gärtner, Florian R and Leunig, Alexander and Pekayvaz, Kami and Nicolai, Leo and Fumagalli, Valeria and Stermann, Julia and Stephan, Felix and David, Christian and Müller, Martin B. and Heyman, Birgitta and Lux, Anja and Da Palma Guerreiro, Alexandra and Frenzel, Lukas P. and Schmidt, Christoph Q. and Dopler, Arthur and Moser, Markus and Chandraratne, Sue and Von Brühl, Marie Luise and Lorenz, Michael and Korff, Thomas and Rudelius, Martina and Popp, Oliver and Kirchner, Marieluise and Mertins, Philipp and Nimmerjahn, Falk and Iannacone, Matteo and Sperandio, Markus and Engelmann, Bernd and Verschoor, Admar and Massberg, Steffen},
  issn         = {1097-4180},
  journal      = {Immunity},
  number       = {9},
  pages        = {2140--2156},
  publisher    = {Elsevier},
  title        = {{Antibodies and complement are key drivers of thrombosis}},
  doi          = {10.1016/j.immuni.2024.08.007},
  volume       = {57},
  year         = {2024},
}

@article{7876,
  abstract     = {In contrast to lymph nodes, the lymphoid regions of the spleen—the white pulp—are located deep within the organ, yielding the trafficking paths of T cells in the white pulp largely invisible. In an intravital microscopy tour de force reported in this issue of Immunity, Chauveau et al. show that T cells perform unidirectional, perivascular migration through the enigmatic marginal zone bridging channels. },
  author       = {Sixt, Michael K and Lämmermann, Tim},
  issn         = {1097-4180},
  journal      = {Immunity},
  number       = {5},
  pages        = {721--723},
  publisher    = {Elsevier},
  title        = {{T cells: Bridge-and-channel commute to the white pulp}},
  doi          = {10.1016/j.immuni.2020.04.020},
  volume       = {52},
  year         = {2020},
}