Neutrophil migration: moving from zebrafish models to human autoimmunity
- Authors
- Shelef, M.A., Tauzin, S., and Huttenlocher, A.
- ID
- ZDB-PUB-131113-12
- Date
- 2013
- Source
- Immunological reviews 256(1): 269-281 (Review)
- Registered Authors
- Huttenlocher, Anna
- Keywords
- neutrophil, migration, autoimmune, Lyn, Rac2, SHIP
- MeSH Terms
-
- Animals
- Autoimmune Diseases/immunology
- Autoimmunity
- Cell Movement/physiology*
- Humans
- Microtubules/metabolism
- Neutrophils/physiology*
- Phosphoric Monoester Hydrolases/metabolism
- Zebrafish
- rac GTP-Binding Proteins/metabolism
- src-Family Kinases/metabolism
- PubMed
- 24117827 Full text @ Immunol. Rev.
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.