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Medfødt immunitet, autoimmunitet og autoinflammation
Engelsk titel: Innate immunity, autoimmunity and autoinflammation Läs online Författare: Bendtzen, Klaus Språk: Dan Antal referenser: 14 Dokumenttyp: Artikel UI-nummer: 11091958

Tidskrift

Ugeskrift for Laeger 2011;173(38)2337-40 ISSN 0041-5782 E-ISSN 1603-6824 KIBs bestånd av denna tidskrift

Sammanfattning

T and B lymphocytes of the acquired immune system are functionally superimposed on the evolutionary old innate immune system. The latter recognizes conserved microbial structures through pattern recognition receptors (PRR) and are coactivated by "danger" signals through cytoplasmic PRR termed NOD-like receptors (NLR). These signals include nuclear fragments released by stressed or dying cells. NLR-signalling activates the enzyme caspase-1, which is required for release of pro-inflammatory cytokines such as interleukin (IL)-1?, IL-18 and IL-33. Dysfunction of innate immunity is central to autoinflammation and may contribute to autoimmunity.