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The role of Toll-like receptor signaling in the macrophage response to implanted materials

Published online by Cambridge University Press:  06 December 2019

Laura A. McKiel
Affiliation:
Department of Chemical Engineering, Queen's University, Dupuis Hall, Room 201, 19 Division St, Kingston, Ontario, CanadaK7K 3N6
Kimberly A. Woodhouse
Affiliation:
Department of Chemical Engineering, Queen's University, Dupuis Hall, Room 201, 19 Division St, Kingston, Ontario, CanadaK7K 3N6
Lindsay E. Fitzpatrick*
Affiliation:
Department of Chemical Engineering, Queen's University, Dupuis Hall, Room 201, 19 Division St, Kingston, Ontario, CanadaK7K 3N6
*
Address all correspondence to Lindsay E. Fitzpatrick at lindsay.fitzpatrick@queensu.ca
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Abstract

Inflammation is facilitated largely by macrophages and other white blood cells, which recognize and respond to evolutionarily conserved damage-associated molecular patterns that are released upon tissue injury and cell stress. Damage-associated molecular patterns are known to bind Toll-like receptors (TLRs) and initiate inflammatory responses through MyD88-dependent NF-κB signaling. Biomaterial implantation activates the innate immune system, resulting in a chronic inflammatory response known as a foreign body reaction (FBR). In this review, the authors discuss the current understanding of damage-initiated TLR signaling in the FBR and the significance of this response in the success of implanted devices.

Type
Prospective Articles
Copyright
Copyright © Materials Research Society 2019

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