@article{12119,
  abstract     = {Intravascular neutrophils and platelets collaborate in maintaining host integrity, but their interaction can also trigger thrombotic complications. We report here that cooperation between neutrophil and platelet lineages extends to the earliest stages of platelet formation by megakaryocytes in the bone marrow. Using intravital microscopy, we show that neutrophils “plucked” intravascular megakaryocyte extensions, termed proplatelets, to control platelet production. Following CXCR4-CXCL12-dependent migration towards perisinusoidal megakaryocytes, plucking neutrophils actively pulled on proplatelets and triggered myosin light chain and extracellular-signal-regulated kinase activation through reactive oxygen species. By these mechanisms, neutrophils accelerate proplatelet growth and facilitate continuous release of platelets in steady state. Following myocardial infarction, plucking neutrophils drove excessive release of young, reticulated platelets and boosted the risk of recurrent ischemia. Ablation of neutrophil plucking normalized thrombopoiesis and reduced recurrent thrombosis after myocardial infarction and thrombus burden in venous thrombosis. We establish neutrophil plucking as a target to reduce thromboischemic events.},
  author       = {Petzold, Tobias and Zhang, Zhe and Ballesteros, Iván and Saleh, Inas and Polzin, Amin and Thienel, Manuela and Liu, Lulu and Ul Ain, Qurrat and Ehreiser, Vincent and Weber, Christian and Kilani, Badr and Mertsch, Pontus and Götschke, Jeremias and Cremer, Sophie and Fu, Wenwen and Lorenz, Michael and Ishikawa-Ankerhold, Hellen and Raatz, Elisabeth and El-Nemr, Shaza and Görlach, Agnes and Marhuenda, Esther and Stark, Konstantin and Pircher, Joachim and Stegner, David and Gieger, Christian and Schmidt-Supprian, Marc and Gärtner, Florian R and Almendros, Isaac and Kelm, Malte and Schulz, Christian and Hidalgo, Andrés and Massberg, Steffen},
  issn         = {1074-7613},
  journal      = {Immunity},
  keywords     = {Infectious Diseases, Immunology, Immunology and Allergy},
  number       = {12},
  pages        = {2285--2299.e7},
  publisher    = {Elsevier},
  title        = {{Neutrophil “plucking” on megakaryocytes drives platelet production and boosts cardiovascular disease}},
  doi          = {10.1016/j.immuni.2022.10.001},
  volume       = {55},
  year         = {2022},
}

@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},
}

@article{664,
  abstract     = {Immune cells communicate using cytokine signals, but the quantitative rules of this communication aren't clear. In this issue of Immunity, Oyler-Yaniv et al. (2017) suggest that the distribution of a cytokine within a lymphatic organ is primarily governed by the local density of cells consuming it.},
  author       = {Assen, Frank P and Sixt, Michael K},
  issn         = {1074-7613},
  journal      = {Immunity},
  number       = {4},
  pages        = {519 -- 520},
  publisher    = {Cell Press},
  title        = {{The dynamic cytokine niche}},
  doi          = {10.1016/j.immuni.2017.04.006},
  volume       = {46},
  year         = {2017},
}