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Mol Immunol. 2015 Feb;63(2):143-52. doi: 10.1016/j.molimm.2014.05.008. Epub 2014 Jun 17.

Toll-like receptor co-receptors as master regulators of the immune response.

Author information

1
University of Milano-Bicocca, Department of Biotechnology and Biosciences, P.zza della Scienza 2, 20126, Milan, Italy.
2
University of Milano-Bicocca, Department of Biotechnology and Biosciences, P.zza della Scienza 2, 20126, Milan, Italy; Children's Hospital Boston, Division of Gastroenterology, Harvard Medical School, 300 Longwood Ave, Enders, Boston, MA 02115, United States of America. Electronic address: ivan.zanoni@unimib.it.

Abstract

Pattern recognition receptors (PRRs) are generally recognized as the initiators of all immune responses. PRRs bind molecular patterns associated with microorganisms or endogenous mediators released by stressed tissues. Upon ligand binding, PRRs induce the activation of an inflammatory process that ultimately leads to pathogen clearance or restoration of tissue homeostasis. PRRs govern these processes, regulating the activation of a complex network of transcription factors able to induce the appropriate immune response to a specific ligand. Toll-like-receptors (TLRs) are the first and best characterized PRR family, and for a long period of time they were believed to be autonomous proteins able to recognize and initiate all the immune response to a given stimulus. Recently this view was challenged by the discovery that so-called TLR co-receptors, such as CD14 and CD36, not only favor TLR-dependent signaling but can also transduce their own signal in a TLR-independent manner. Here we will discuss the capacity of TLR co-receptors to bind different microbial and endogenous ligands and to integrate TLR functions inducing specific signaling modules.

KEYWORDS:

Accessory molecules; CD14; CD36; DAMP; MAMP; Toll like receptor

PMID:
24951397
DOI:
10.1016/j.molimm.2014.05.008
[Indexed for MEDLINE]
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