@article{19928,
  abstract     = {Patho-mechanistic origins of ulcerative colitis are still poorly understood. The actin cross-linker filamin A (FLNA) impacts cellular responses through interaction with cytosolic proteins. Posttranscriptional A-to-I editing generates two forms of FLNA: genome-encoded FLNAQ and FLNAR. FLNA is edited in colon fibroblasts, smooth muscle cells, and endothelial cells. We found that the FLNA editing status determines colitis severity. Editing was highest in healthy colons and reduced during murine and human colitis. Mice that exclusively express FLNAR were highly resistant to DSS-induced colitis, whereas fully FLNAQ animals developed severe inflammation. While the genetic induction of FLNA editing influenced transcriptional states of structural cells and microbiome composition, we found that FLNAR exerts protection specifically via myeloid cells, which are physiologically unedited. Introducing fixed FLNAR did not hamper cell migration but reduced macrophage inflammation and rendered neutrophils less prone to NETosis. Thus, loss of FLNA editing correlates with colitis severity, and targeted editing of myeloid cells serves as a novel therapeutic approach in intestinal inflammation.},
  author       = {Gawish, Riem and Varada, Rajagopal and Deckert, Florian and Hladik, Anastasiya and Steinbichl, Linda and Cimatti, Laura and Milanovic, Katarina and Jain, Mamta and Torgasheva, Natalya and Tanzer, Andrea and De Paepe, Kim and Van De Wiele, Tom and Hausmann, Bela and Lang, Michaela and Pechhacker, Martin and Ibrahim, Nahla and De Vries, Ingrid and Brostjan, Christine and Sixt, Michael K and Gasche, Christoph and Boon, Louis and Berry, David and Jantsch, Michael F. and Pereira, Fatima C. and Vesely, Cornelia},
  issn         = {1540-9538},
  journal      = {Journal of Experimental Medicine},
  number       = {9},
  publisher    = {Rockefeller University Press},
  title        = {{Filamin A editing in myeloid cells reduces intestinal inflammation and protects from colitis}},
  doi          = {10.1084/jem.20240109},
  volume       = {222},
  year         = {2025},
}

@article{6497,
  abstract     = {T cells are actively scanning pMHC-presenting cells in lymphoid organs and nonlymphoid tissues (NLTs) with divergent topologies and confinement. How the T cell actomyosin cytoskeleton facilitates this task in distinct environments is incompletely understood. Here, we show that lack of Myosin IXb (Myo9b), a negative regulator of the small GTPase Rho, led to increased Rho-GTP levels and cell surface stiffness in primary T cells. Nonetheless, intravital imaging revealed robust motility of Myo9b−/− CD8+ T cells in lymphoid tissue and similar expansion and differentiation during immune responses. In contrast, accumulation of Myo9b−/− CD8+ T cells in NLTs was strongly impaired. Specifically, Myo9b was required for T cell crossing of basement membranes, such as those which are present between dermis and epidermis. As consequence, Myo9b−/− CD8+ T cells showed impaired control of skin infections. In sum, we show that Myo9b is critical for the CD8+ T cell adaptation from lymphoid to NLT surveillance and the establishment of protective tissue–resident T cell populations.},
  author       = {Moalli, Federica and Ficht, Xenia and Germann, Philipp and Vladymyrov, Mykhailo and Stolp, Bettina and de Vries, Ingrid and Lyck, Ruth and Balmer, Jasmin and Fiocchi, Amleto and Kreutzfeldt, Mario and Merkler, Doron and Iannacone, Matteo and Ariga, Akitaka and Stoffel, Michael H. and Sharpe, James and Bähler, Martin and Sixt, Michael K and Diz-Muñoz, Alba and Stein, Jens V.},
  issn         = {1540-9538},
  journal      = {The Journal of Experimental Medicine},
  number       = {7},
  pages        = {1869–1890},
  publisher    = {Rockefeller University Press},
  title        = {{The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells}},
  doi          = {10.1084/jem.20170896},
  volume       = {2015},
  year         = {2018},
}

@article{3942,
  abstract     = {Recent in vitro studies have suggested a role for sialylation in chemokine receptor binding to its ligand (Bannert, N., S. Craig, M. Farzan, D. Sogah, N.V. Santo, H. Choe, and J. Sodroski. 2001. J. Exp. Med. 194:1661-1673). This prompted us to investigate chemokine-induced leukocyte adhesion in inflamed cremaster muscle venules of alpha2,3 sialyltransferase (ST3Gal-IV)-deficient mice. We found a marked reduction in leukocyte adhesion to inflamed microvessels upon injection of the CXCR2 ligands CXCL1 (keratinocyte-derived chemokine) or CXCL8 (interleukin 8). In addition, extravasation of ST3Gal-IV(-/-) neutrophils into thioglycollate-pretreated peritoneal cavities was significantly decreased. In vitro assays revealed that CXCL8 binding to isolated ST3Gal-IV(-/-) neutrophils was markedly impaired. Furthermore, CXCL1-mediated adhesion of ST3Gal-IV(-/-) leukocytes at physiological flow conditions, as well as transendothelial migration of ST3Gal-IV(-/-) leukocytes in response to CXCL1, was significantly reduced. In human neutrophils, enzymatic desialylation decreased binding of CXCR2 ligands to the neutrophil surface and diminished neutrophil degranulation in response to these chemokines. In addition, binding of alpha2,3-linked sialic acid-specific Maackia amurensis lectin II to purified CXCR2 from neuraminidase-treated CXCR2-transfected HEK293 cells was markedly impaired. Collectively, we provide substantial evidence that sialylation by ST3Gal-IV significantly contributes to CXCR2-mediated leukocyte adhesion during inflammation in vivo.},
  author       = {Frommhold, David and Ludwig, Andreas and Bixel, M Gabriele and Zarbock, Alexander and Babushkina, Inna and Weissinger, Melitta and Cauwenberghs, Sandra and Ellies, Lesley and Marth, Jamey and Beck Sickinger, Annette and Sixt, Michael K and Lange Sperandio, Bärbel and Zernecke, Alma and Brandt, Ernst and Weber, Christian and Vestweber, Dietmar and Ley, Klaus and Sperandio, Markus},
  issn         = {1540-9538},
  journal      = {The Journal of Experimental Medicine},
  number       = {6},
  pages        = {1435 -- 1446},
  publisher    = {Rockefeller University Press},
  title        = {{Sialyltransferase ST3Gal-IV controls CXCR2-mediated firm leukocyte arrest during inflammation}},
  doi          = {10.1084/jem.20070846},
  volume       = {205},
  year         = {2008},
}