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Innate immunity and autoimmune disease [Editorial]

Wong, Florence Susan and Wen, Li 2009. Innate immunity and autoimmune disease [Editorial]. Current Molecular Medicine 9 (1) , pp. 1-3. 10.2174/156652409787314462

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Abstract

The immune system provides a vital protective system for living organisms from infection. Most organisms from the simplest to the most complex have some form of innate immune system, to provide the relatively non-specific early response against invasion of pathogens. Apart from the physical barriers to infection, the non-specific enzymes such as lysozyme in tears and saliva and anti-bacterial peptides that include defensins, there are an array of cells including natural killer (NK) and natural killer T (NKT) cells, macrophages, γδ T cells, neutrophils, eosinophils, basophils and mast cells that all play an important role in this first line of defence. These cells recognize common patterns of pathogens via a large array of receptors that include the Toll-like receptors (TLR) that recognize both extracellular and intracellular stimuli, the nucleotide oligomerization domain (NOD) like receptors (NLR), RIG-I like receptors (RLR), which are reactive to nucleic acids, and caspase recruitment domain (CARD) proteins, which recognize predominantly intracellular molecules. These receptors signal intracellularly through a number of adaptors, that include Myeloid Differentiation primary response gene 88 (MyD88), MyD88 adaptor-like/ TIR domain containing adaptor protein (MAL), Toll-IL-1-resistance domain containing adaptor inducing interferon beta (TRIF), TRIF-related adaptor molecule (TRAM) and Sterile-alpha and Armadillo motif containing protein (SARM) leading to the activation of NFκB, as reviewed in this issue by Page and colleagues [1]. Recent studies suggest that stimulator of interferon genes (STING) is an endoplasmic reticulum adaptor for RLR [2]. These receptors not only detect pathogens in the external environment, but may also respond to tissue damage and initiate responses to endogenous signals [3]. Cytokines and chemokines produced by the innate cells in early response attract more innate cells and as dendritic cells become involved in endocytosing antigen and traffick to local lymph nodes, an adaptive, more specific response involving T and B cells will be initiated. Although occurring sequentially, the immune response is a very complex and inter-related series of events. Although innate and adaptive immune responses are traditionally thought of as being somewhat compartmentalized, it is now clear that these two types of immune responses are highly interconnected at many levels. In this light, it is not surprising that this interaction will not only be seen in the context of infection but also in other settings where chronic inflammation is prominent, such as in autoimmune disease. Many autoimmune diseases occur through adaptive immune response effectors against autoantigens. Both selfreactive T cells and autoantibody producing B cells are found in the diseases that include multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, type 1 diabetes and autoimmune liver disorders. Whether the role of autoreactive B or T cells is more dominant depends on the individual disease. Genetic susceptibility has been identified in many autoimmune diseases and certain HLA types predispose to different diseases. However, environmental factors play a critical role in determining whether susceptible individuals develop autoimmune disease, although the nature of these factors is not well defined. Increasing evidence suggests that both the external as well as the internal environment are important in disease onset and progression.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Systems Immunity Research Institute (SIURI)
Subjects: R Medicine > R Medicine (General)
Publisher: Bentham Science Publishers
ISSN: 1566-5240
Last Modified: 04 Jun 2017 03:11
URI: http://orca.cf.ac.uk/id/eprint/17809

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