Vicious circle: systemic autoreactivity in Ro52/TRIM21-deficient mice.
Dysregulated innate responses, particularly excessive activation of interferon (IFN) pathways, have been implicated in the development of autoimmune pathologies. Autoreactivity frequently targets IFN-inducible genes such as the Ro autoantigens, which ubiquitinate and inhibit interferon regulatory factors (IRFs). A new study validates the role of these common autoantigens in preventing autoimmunity. The findings reveal that injury-induced systemic autoimmune disease is exacerbated in the absence of Ro52/Trim21 and is driven by the IL-23-Th17 pathway.
Bolland
Silvia
S
Laboratory of Immunogenetics, National Institute of Allergy and Infectious Disease, National Institutes of Health, Rockville MD 20852, USA. SBolland@niaid.nih.gov
Garcia-Sastre
Adolfo
A
D000818:Animals; D001327:Autoimmune Diseases / Q000209:etiology / Q000235:genetics / Q000276:immunology; D015551:Autoimmunity / Q000235:genetics; D016207:Cytokines / Q000235:genetics; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation / Q000235:genetics / Q000276:immunology; D051379:Mice; D018345:Mice, Knockout; D018448:Models, Immunological; D012261:Ribonucleoproteins / Q000172:deficiency* / Q000235:genetics; D000099207:SS-A Antigen
D016207:Cytokines; D012261:Ribonucleoproteins; D000099207:SS-A Antigen