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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:1085.)
© 2005 American Heart Association, Inc.

Editorials

Toll To Be Paid at the Gateway to the Vessel Wall

Göran K. Hansson; Kristina Edfeldt

From the Center for Molecular Medicine and Department of Medicine, Karolinska Institute, Stockholm, Sweden.

Correspondence to Göran K. Hansson, Center for Molecular Medicine and Department of Medicine, Karolinska University Hospital L8:03 Karolinska Institute SE-17176 Stockholm, Sweden. E-mail goran.hansson@cmm.ki.se

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The innate immune defense is ready to combat invading microbes whenever they invade our inner territories. Innate immunity consists of soluble molecules and cell-bound receptors, all of which are encoded in the germline DNA. This contrasts with the adaptive immune system, the molecular components of which are generated by somatic rearrangement processes. In atherosclerosis research, much interest has been focused on a soluble component of innate immunity, the acute phase protein C-reactive protein (CRP). Other members of the innate immune family are also involved in the atherosclerotic process, including the complement cascade, the antimicrobial peptides, and the pattern recognition receptors (PRR).

See pages 1213 and 1220

The large group of PRRs contains several families of receptors. Their common denominator is a broad specificity with a capacity to bind many different macromolecules produced by invading microbes. The first PRRs to be discovered were the scavenger receptors (ScR), which were identified as transmembrane receptors binding lipopolysaccharide (LPS) of endotoxins, acetylated LDL, and certain polynucleotides. Michael Brown and Joseph Goldstein discovered ScR in 1979,¹ and the first one of them, SR-A, was cloned in 1990.²

The next step in PRR discovery came from an entirely different line of research. Christiane Nüsslein-Volhard of the Max Planck Institute in Tübingen analyzed mutations in fruit flies. In 1985, she saw a weird-looking fly larva in which the ventral portion of the body was underdeveloped. Her spontaneous comment was "Das war ja toll!" meaning "That was weird!" and she coined the name Toll for the mutated gene. . . . [Full Text of this Article]

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