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CD46 Plasticity and Its Inflammatory Bias in Multiple Sclerosis

  • REVIEW
  • Published:
Archivum Immunologiae et Therapiae Experimentalis Aims and scope

Abstract

Known as a link to the adaptive immune system, a complement regulator, a “pathogen magnet” and more recently as an inducer of autophagy, CD46 is the human receptor that refuses to be put in a box. This review summarizes the current roles of CD46 during immune responses and highlights the role of CD46 as both a promoter and attenuator of the immune response. In patients with multiple sclerosis (MS), CD46 responses are overwhelmingly pro-inflammatory with notable defects in cytokine and chemokine production. Understanding the role of CD46 as an inflammatory regulator is a distant goal considering the darkness in which its regulatory mechanisms reside. Further research into the regulation of CD46 expression through its internalization and processing will undoubtedly extend our knowledge of how the balance is tipped in favor of inflammation in MS patients.

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Abbreviations

ADAM:

A disintegrin and metalloproteinase

BBB:

Blood brain barrier

CTF:

C-terminal transmembrane fragment

DC:

Dendritic cell

mDCs:

Myeloid DCs

EAE:

Experimental autoimmune encephalomyelitis

Tregs:

T-regulatory cells

MMP:

Matrix metalloproteinase

MS:

Multiple sclerosis

RRMS:

Relapsing-remitting MS

MV:

Measles virus

PγS:

Presenilin-γ-secretase

VLA-4:

Very late activation antigen 4

VCAM-1:

Vascular cell adhesion molecule-1

HHV-6:

Herpes virus 6

TCR:

T cell receptor

CTLs:

Cytotoxic T lymphocytes

NK:

Natural killer

MTOC:

Microtubule organization centre

APP:

Amyloid precursor protein

LPS:

Lipopolysaccharide

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Acknowledgments

This work was supported by a research grant from the MS society (UK) to A. L. Astier (859/7).

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Correspondence to Anne L. Astier.

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Ni Choileain, S., Astier, A.L. CD46 Plasticity and Its Inflammatory Bias in Multiple Sclerosis. Arch. Immunol. Ther. Exp. 59, 49–59 (2011). https://doi.org/10.1007/s00005-010-0109-7

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  • DOI: https://doi.org/10.1007/s00005-010-0109-7

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