Recruitment of CD16+ monocytes to endothelial cells in response to LPS-treatment and concomitant TNF release is regulated by CX3CR1 and interfered by soluble fractalkine
详细信息 查看全文
- 作者：Knut Rennerta ; b ; Kerstin Heisigc ; Marko Groegera ; b ; Maria Wallertd ; Harald Funkec ; Stefan Lorkowskid ; e ; Otmar Hubera ; b ; Alexander S. Mosiga ; b ; alexander.mosig@med.uni-jena.de" class="auth_mail" title="E-mail the corresponding author
- 关键词：7AAD ; 7-aminoactinomycin ; ADAM17 ; a disintegrin and metallopeptidase domain 17 ; BB94 ; batimastat ; CBA ; cytometric bead array ; CCR2 ; chemokine (C-C motif) receptor 2 ; CD14 ; monocyte differentiation antigen CD14 ; CD16 ; Fcγ receptor III (FcγRIII) ; CX3CR1 ; CX3C chemokine receptor 1 ; FKN ; fractalkine ; CX3CL1 ; HLA-DR ; major histocompatibility complex class II ; DR ; HUVEC ; human umbilical vein endothelial cells ; ICAM-1 ; intercellular adhesion molecule 1 ; IL-1β ; interleukin-1β ; LPS ; lipopolysaccharide ; L
- 刊名：Cytokine
- 出版年：2016
- 出版时间：July 2016
- 年：2016
- 卷：83
- 期：Complete
- 页码：41-52
- 全文大小：2429 K
文摘
- •
CD16+ monocytes are efficiently recruited to endothelial cells (EC) in presence of LPS.
- •
TNF release is amplified upon CX3CR1-dependet CD16+ monocyte adhesion to EC.
- •
Fractalkine shed by CD16+ monocytes interferes with CD3CR1-dependent cell adhesion.
- •
Shedding of fractalkine thereby balances TNF release and CD16+ monocyte recruitment.