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

24 Citations (Scopus)

20 Downloads (Pure)

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
Early online date	19 Mar 2016
DOIs	https://doi.org/10.1016/j.micinf.2016.03.007
Publication status	Published - Jul 2016

Bibliographical note

Acknowledgements
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.

Keywords

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

Access to Document

10.1016/j.micinf.2016.03.007Licence: CC BY

20Figure 3Accepted author manuscript, 50 KBLicence: CC BY
Signalling through MyD88 drives surface expression of the mycobacterial receptors MCL (Clecsf8, Clec4d) and Mincle (Clec4e) following microbial stimulation
© 2016 The Authors. Published by Elsevier Masson SAS on behalf of Institut Pasteur. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
Final published version, 589 KBLicence: CC BY

BD LSR Fortessa
Andrea Holme (Manager)
Iain Fraser Cytometry Centre
Research Facilities: Equipment
Iain Fraser Cytometry Centre
Andrea Holme (Manager), Linda Duncan (Senior Application Scientist), Ailsa Laird (Technician) & Kate Burgoyne (Technician)
Institute of Medical Sciences
Research Facilities: Facility

Cite this

@article{26e74b39a1d1407ebe106f2b8272888d,

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.",

keywords = "C-type lectin receptor, Clec4d, Dectin-3, Clec4e, MyD88, TLR signalling",

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 = "Acknowledgements 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.",

year = "2016",

month = jul,

doi = "10.1016/j.micinf.2016.03.007",

language = "English",

volume = "18",

pages = "505--509",

journal = "Microbes and Infection",

issn = "1286-4579",

publisher = "Elsevier Masson SAS",

number = "7-8",

}

TY - JOUR

T1 - Signalling through MyD88 drives surface expression of the mycobacterial receptors MCL (Clecsf8, Clec4d) and Mincle (Clec4e) following microbial stimulation

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 - Acknowledgements 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.

PY - 2016/7

Y1 - 2016/7

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.

KW - C-type lectin receptor

KW - Clec4d

KW - Dectin-3

KW - Clec4e

KW - MyD88

KW - TLR signalling

U2 - 10.1016/j.micinf.2016.03.007

DO - 10.1016/j.micinf.2016.03.007

M3 - Article

SN - 1286-4579

VL - 18

SP - 505

EP - 509

JO - Microbes and Infection

JF - Microbes and Infection

IS - 7-8

ER -

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

Abstract

Bibliographical note

Keywords

Access to Document

Fingerprint

Equipment

BD LSR Fortessa

Iain Fraser Cytometry Centre

Cite this