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

doi:10.1016/j.micinf.2016.03.007

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 journal › Article › peer-review

23 Citations (Scopus)

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 language	English
Pages (from-to)	505-509
Number of pages	5
Journal	Microbes and Infection
Volume	18
Issue number	7-8
DOIs	https://doi.org/10.1016/j.micinf.2016.03.007
Publication status	Published - Jul 1 2016

All Science Journal Classification (ASJC) codes

Microbiology
Immunology
Infectious Diseases

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.micinf.2016.03.007

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

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.",

author = "Bernhard Kerscher and Dambuza, {Ivy M.} and Maria Christofi and Reid, {Delyth M.} and Sho Yamasaki and Willment, {Janet A.} and Brown, {Gordon D.}",

note = "Funding Information: We would like to thank the staff of the animal facility for their support and care for our animals. Funding was provided by the Wellcome Trust ( 102705 ) and Medical Research Council (UK) ( MR/J004820/1 ) and a University of Aberdeen Studentship to BK. Publisher Copyright: {\textcopyright} 2016 The Authors",

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AU - Kerscher, Bernhard

AU - Dambuza, Ivy M.

AU - Christofi, Maria

AU - Reid, Delyth M.

AU - Yamasaki, Sho

AU - Willment, Janet A.

AU - Brown, Gordon D.

N1 - Funding Information: We would like to thank the staff of the animal facility for their support and care for our animals. Funding was provided by the Wellcome Trust ( 102705 ) and Medical Research Council (UK) ( MR/J004820/1 ) and a University of Aberdeen Studentship to BK. Publisher Copyright: © 2016 The Authors

PY - 2016/7/1

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N2 - 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.

AB - 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.

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

Abstract

All Science Journal Classification (ASJC) codes

UN SDGs

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