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

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 Mi...

Full description

Bibliographic Details
Main Authors:	Kerscher, Bernhard, Dambuza, Ivy M., Christofi, Maria, Reid, Delyth M., Yamasaki, Sho, Willment, Janet A., Brown, Gordon D.
Format:	Online
Language:	English
Published:	Elsevier 2016
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4936759/

id	pubmed-4936759
recordtype	oai_dc
spelling	pubmed-49367592016-07-14 Signalling through MyD88 drives surface expression of the mycobacterial receptors MCL (Clecsf8, Clec4d) and Mincle (Clec4e) following microbial stimulation Kerscher, Bernhard Dambuza, Ivy M. Christofi, Maria Reid, Delyth M. Yamasaki, Sho Willment, Janet A. Brown, Gordon D. Short Communication 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. Elsevier 2016 /pmc/articles/PMC4936759/ /pubmed/27005451 http://dx.doi.org/10.1016/j.micinf.2016.03.007 Text en © 2016 The Authors http://creativecommons.org/licenses/by/4.0/ This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Kerscher, Bernhard Dambuza, Ivy M. Christofi, Maria Reid, Delyth M. Yamasaki, Sho Willment, Janet A. Brown, Gordon D.
spellingShingle	Kerscher, Bernhard Dambuza, Ivy M. Christofi, Maria Reid, Delyth M. Yamasaki, Sho Willment, Janet A. Brown, Gordon D. Signalling through MyD88 drives surface expression of the mycobacterial receptors MCL (Clecsf8, Clec4d) and Mincle (Clec4e) following microbial stimulation
author_facet	Kerscher, Bernhard Dambuza, Ivy M. Christofi, Maria Reid, Delyth M. Yamasaki, Sho Willment, Janet A. Brown, Gordon D.
author_sort	Kerscher, Bernhard
title	Signalling through MyD88 drives surface expression of the mycobacterial receptors MCL (Clecsf8, Clec4d) and Mincle (Clec4e) following microbial stimulation
title_short	Signalling through MyD88 drives surface expression of the mycobacterial receptors MCL (Clecsf8, Clec4d) and Mincle (Clec4e) following microbial stimulation
title_full	Signalling through MyD88 drives surface expression of the mycobacterial receptors MCL (Clecsf8, Clec4d) and Mincle (Clec4e) following microbial stimulation
title_fullStr	Signalling through MyD88 drives surface expression of the mycobacterial receptors MCL (Clecsf8, Clec4d) and Mincle (Clec4e) following microbial stimulation
title_full_unstemmed	Signalling through MyD88 drives surface expression of the mycobacterial receptors MCL (Clecsf8, Clec4d) and Mincle (Clec4e) following microbial stimulation
title_sort	signalling through myd88 drives surface expression of the mycobacterial receptors mcl (clecsf8, clec4d) and mincle (clec4e) following microbial stimulation
description	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.
publisher	Elsevier
publishDate	2016
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4936759/
_version_	1613605705719218176

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

Similar Items