The role of neutrophils and G‐CSF in DNFB‐induced contact hypersensitivity in mice

Immunity, Inflammation and Disease

Anne Deen Christensen¹  Søren Skov² 

[1] Department of Immunopharmacology, Novo Nordisk A/S, Måløv, Denmark;Department of Veterinary Disease Biology, Section for Experimental Animal Models, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg C, Denmark

关键词: Contact hypersensitivity;    neutrophil mobilization G‐CSF;    and neutrophils;   

DOI  :  10.1002/iid3.16

来源: Wiley

【 摘 要 】

Abstract

Neutrophils are thought to play an important role during contact hypersensitivity (CHS) in mice, a notion which is supported by studies in which neutrophils are depleted by monoclonal antibodies (mAb). Here, we show that administration of the commonly used anti-mouse Ly6G/C mAb (clone RB6.8C5) leads to depletion of not only neutrophils but also a population of monocytes and macrophages. In contrast, depletion using a Ly6G-specific mAb (clone 1A8) only leads to depletion of neutrophils. We demonstrate that the anti-Ly6G/C mAb suppresses the inflammatory response to a higher extent than the anti-Ly6G mAb suggesting that the impact of neutrophil-depletion in the CHS model may have been overstated when based on protocols using the anti-Ly6G/C mAb. Still, the role of neutrophils in CHS is substantiated as we demonstrate that G-CSF is an important regulator of neutrophil mobilization and effector function in CHS. Indeed, G-CSF was detectable both in the inflamed tissue and in serum during the immune response and we show that blocking G-CSF results in a reduced number of neutrophils in the blood and an attenuation of the ear-swelling response in the tissue.

In conclusion, this study supports that neutrophils are important drivers of inflammation in the DNFB-induced CHS model and shows that G-CSF is a significant factor in mobilizing neutrophils during the response.

【 授权许可】

CC BY   
© 2014 The Authors. Immunity, Inflammation and Disease Published by John Wiley & Sons Ltd.

Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.