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The relationship between infections and autoimmune inflammation is of paramount importance in all chronic inflammatory diseases.1 The crucial step is the interaction between the Toll-like receptor family and bacterial components, which can lead to activation of phagocytic and dendritic cells.2,3 Whether bacterial components may indeed reactivate autoimmune inflammation is at present still unclear. However, it is well known that oligonucleotides containing unmethylated CpG sequences (CpG-ODN), while stimulating bacterial DNA, might have immunostimulatory activity.3 We have recently presented data suggesting that moderate infections such as upper-lower respiratory or urinary tracts infections may reactivate rheumatoid arthritis (RA) in patients receiving etanercept.4
There is evidence in experimental animals2,3 that Toll-like receptor 4 (activated by lipolysaccharide (LPS)) can induce a cytokine response, whereas Toll-like receptor 9, activated by CpG-ODN, induces mononuclear cell activation in a much more restricted manner. Especially in humans, …
Footnotes
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B Tolusso and M Fabris contributed equally to this work.