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Front Cell Infect Microbiol. 2014 May 20;4:55. doi: 10.3389/fcimb.2014.00055. eCollection 2014.

Phagosomal TLR signaling upon Borrelia burgdorferi infection.

Author information

1
Department of Pediatrics, University of Connecticut Health Center Farmington, CT, USA ; Division of Infectious Diseases, Connecticut Children's Medical Center Hartford, CT, USA.
2
Department of Pediatrics, University of Connecticut Health Center Farmington, CT, USA.
3
Department of Molecular Biology and Biophysics, University of Connecticut Health Center Farmington, CT, USA.
4
Department of Pediatrics, University of Connecticut Health Center Farmington, CT, USA ; Division of Infectious Diseases, Connecticut Children's Medical Center Hartford, CT, USA ; Department of Immunology, University of Connecticut Health Center Farmington, CT, USA.

Abstract

Internalization and degradation of live Bb within phagosomal compartments of monocytes, macrophages and dendritic cells (DCs), allows for the release of lipoproteins, nucleic acids and other microbial products, triggering a broad and robust inflammatory response. Toll-like receptors (TLRs) are key players in the recognition of spirochetal ligands from whole viable organisms (i.e., vita-PAMPs). Herein we will review the role of endosomal TLRs in the response to the Lyme disease spirochete.

KEYWORDS:

Borrelia burgdorferi; Lyme disease; innate immunity; phagosomal signaling; toll-like receptors

PMID:
24904837
PMCID:
PMC4033037
DOI:
10.3389/fcimb.2014.00055
[Indexed for MEDLINE]
Free PMC Article

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