Infections as triggers of flares in systemic autoimmune diseases: novel innate immunity mechanisms

摘要

Purpose of review The innate immune response (IIR) has to be immediate facing pathogens, and effective to induce a long-lasting adaptive immunity and immune memory. In genetically susceptible individuals, beyond a first defense, a chronically activated by infections IIR may represent a trigger for the onset or flares in systemic autoimmune diseases. This article reviews the recent scientific literature in this regard and highlights the key issues needing investigation. Recent findings Thanks to its high specificity mediated by pattern recognition receptors, the IIR is not called unspecific anymore. The discovery of these increasingly accurate recognizing molecular mechanisms has also evidenced their involvement in breaking self-immune tolerance and to maintain chronic inflammation in autoimmune responses. Neutrophil extracellular traps (NETS) as the main source of antinuclear antibodies; the 'neutrophils-pDC activation loop' theory; and the Th1/Th2/Th17 misbalances induced by microbial products because of chronically activated innate immune cells, are some of the recent uncovered IIR origins involved in infectious-induced systemic autoimmune diseases. A deeper understanding of the genetic predisposition and the pathogen-derived factors responsible to exacerbate the IIR might potentially provide therapeutic targets to counteract flares in systemic autoimmune diseases.