Signalling through MyD88 drives surface expression of the mycobacterial receptors MCL (Clecsf8, Clec4d) and Mincle (Clec4e) following microbial stimulation

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• 作者：Bernhard Kerscher^a ; Ivy M. Dambuza^a ; Maria Christofi^a ; Delyth M. Reid^a ; Sho Yamasaki^b ; Janet A. Willment^a ; ^{janet.willment@abdn.ac.uk" class="auth_mail" title="E-mail the corresponding author} ; Gordon D. Brown^a ; ^{gordon.brown@abdn.ac.uk" class="auth_mail" title="E-mail the corresponding author}
• 关键词：C-type lectin receptor ; Clec4d ; Dectin-3 ; Clec4e ; MyD88 ; TLR signalling
• 刊名：Microbes and Infection
• 出版年：2016
• 出版时间：July-August 2016
• 年：2016
• 卷：18
• 期：7-8
• 页码：505-509
• 全文大小：588 K

文摘

The heterodimeric mycobacterial receptors, macrophage C-type lectin (MCL) and macrophage inducible C-type lectin (Mincle), are upregulated at the cell surface following microbial challenge, but the mechanisms underlying this response are unclear. Here we report that microbial stimulation triggers Mincle expression through the myeloid differentiation primary response gene 88 (MyD88) pathway; a process that does not require MCL. Conversely, we show that MCL is constitutively expressed but retained intracellularly until Mincle is induced, whereupon the receptors form heterodimers which are translocated to the cell surface. Thus this “two-step” model for induction of these key receptors provides new insights into the underlying mechanisms of anti-mycobacterial immunity.