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Neutrophil migration: moving from zebrafish models to human autoimmunity
Author(s) -
Shelef Miriam A.,
Tauzin Sebastien,
Huttenlocher Anna
Publication year - 2013
Publication title -
immunological reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.839
H-Index - 223
eISSN - 1600-065X
pISSN - 0105-2896
DOI - 10.1111/imr.12124
Subject(s) - neutrophil extracellular traps , autoimmunity , immunology , inflammation , biology , zebrafish , chemotaxis , arthritis , autoimmune disease , rheumatoid arthritis , systemic lupus erythematosus , disease , medicine , immune system , antibody , pathology , receptor , genetics , gene
Summary 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.