The chemokine CCL6 promotes innate immunity via immune cell activation and recruitment.
Septic syndrome is a consequence of innate immune failure. Recent studies showed that the CC chemokine CCL6 enhanced antimicrobial immunity during experimental sepsis through an unknown mechanism. The present study demonstrates that transgenic CCL6 expression abolishes mortality in a septic peritonitis model via the modulation of resident peritoneal cell activation and, more importantly, through the recruitment of IFN-producing NK cells and killer dendritic cells into the peritoneum. Thus, CCL6 attenuates the immune failure during sepsis, in part, through a protective type 1-cytokine mediated mechanism.
Coelho
Ana L
AL
Department of Pathology, University of Michigan, Ann Arbor, Michigan 48109, USA. analuci@med.umich.edu
Schaller
Matthew A
MA
Benjamim
Claudia F
CF
Orlofsky
Amos Z
AZ
Hogaboam
Cory M
CM
Kunkel
Steven L
SL
D000818:Animals; D002465:Cell Movement / Q000276:immunology*; D002478:Cells, Cultured; D019742:Chemokines, CC / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D003713:Dendritic Cells / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D005260:Female; D007113:Immunity, Innate; D007371:Interferon-gamma / Q000096:biosynthesis / Q000502:physiology; D007694:Killer Cells, Natural / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D008262:Macrophage Activation / Q000276:immunology; D017737:Macrophages, Peritoneal / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D010537:Peritoneum / Q000166:cytology* / Q000276:immunology* / Q000378:metabolism; D010538:Peritonitis / Q000276:immunology / Q000378:metabolism / Q000473:pathology
D019742:Chemokines, CC; C070959:Ccl6 protein, mouse; D007371:Interferon-gamma