Nucleic acids modulate autoimmunity through nucleic-acid-specific toll-like receptors.
Autoimmune diseases are believed to develop mainly from three factors comprising genetic predisposition, environmental factors and immune (dys-) regulation. In this context, specific nucleic acids of exogenous or endogenous origin that signal through nucleic acid-specific Toll-like receptors (TLRs) have gained much research attention. During ongoing autoimmune disease microbial nucleic acids contribute to flares of disease and its aggravation leading to end organ damage, through unfavourable immune modulation. Apart from exogenous sources, nucleic acid molecules of endogenous origin emerge as potential ligands for receptors of host defence, i.e. TLRs. Rapidly accumulating data on the role of nucleic acid-specific TLRs has not only provided insights about their pathogenic potential of endogenous nucleic acid molecules, but is also fuelling the development of novel immunotherapies.
Patole
Prashant S
PS
Medical Policlinic, University of Munich, Germany. hjanders@med.uni-muenchen.de.
Anders
Hans-Joachim
HJ
D000818:Animals; D001327:Autoimmune Diseases / Q000209:etiology / Q000276:immunology* / Q000628:therapy; D015551:Autoimmunity / Q000276:immunology* / Q000502:physiology; D006801:Humans; D008562:Membrane Glycoproteins / Q000276:immunology / Q000378:metabolism; D009696:Nucleic Acids / Q000502:physiology*; D011956:Receptors, Cell Surface / Q000276:immunology* / Q000378:metabolism; D051193:Toll-Like Receptors / Q000378:metabolism / Q000502:physiology*
D008562:Membrane Glycoproteins; D009696:Nucleic Acids; D011956:Receptors, Cell Surface; D051193:Toll-Like Receptors