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Neutrophil migration: moving from zebrafish models to human autoimmunity |
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| Authors: | Miriam A. Shelef Sebastien Tauzin Anna Huttenlocher |
| Affiliation: | 1. Division of Rheumatology, Department of Medicine, University of Wisconsin, Madison, Madison, WI, USA;2. Departments of Pediatrics and Medical Microbiology and Immunology, University of Wisconsin, Madison, Madison, WI, USA;3. Departments of Pediatrics and Medical Microbiology and Immunology, University of Wisconsin, Madison, Madison, WI, USA Correspondence to: Anna Huttenlocher Departments of Pediatrics and Medical Microbiology and Immunology University of Wisconsin 4205 Microbial Sciences Building, 1550 Linden Drive Madison, WI 53706, USA Tel.: +1 608 265 4642 Fax: +1 608 262 8418 e-mail: huttenlocher@wisc.edu |
| Abstract: | There has been a resurgence of interest in the neutrophil's role in autoimmune disease. Classically considered an early responder that dies at the site of inflammation, new findings using live imaging of embryonic zebrafish and other modalities suggest that neutrophils can reverse migrate away from sites of inflammation. These ‘inflammation-sensitized’ neutrophils, as well as the neutrophil extracellular traps and other products made by neutrophils in general, may have many implications for autoimmunity. Here, we review what is known about the role of neutrophils in three different autoimmune diseases: rheumatoid arthritis, systemic lupus erythematosus, and small vessel vasculitis. We then highlight recent findings related to several cytoskeletal regulators that guide neutrophil recruitment including Lyn, Rac2, and SHIP. Finally, we discuss how our improved understanding of the molecules that control neutrophil chemotaxis may impact our knowledge of autoimmunity. |
| Keywords: | neutrophil migration autoimmune Lyn Rac2 SHIP |