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

Bernhard Kerscher, Ivy M Dambuza, Maria Christofi, Delyth M Reid, Sho Yamasaki, Janet A Willment, Gordon D Brown

Research output: Contribution to journalArticle

16 Citations (Scopus)
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Abstract

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.
Original languageEnglish
Pages (from-to)505-509
Number of pages5
JournalMicrobes and Infection
Volume18
Issue number7-8
Early online date19 Mar 2016
DOIs
Publication statusPublished - Jul 2016

Keywords

  • C-type lectin receptor
  • Clec4d
  • Dectin-3
  • Clec4e
  • MyD88
  • TLR signalling

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