.png){kind=icon}
.png){kind=icon}
Return
The multiple pathways to autoimmunity
.png){kind=icon}
OA
AI
DOI：10.1038/ni.3731.png)
.png){kind=icon}
.png){kind=icon}
Share.png){kind=icon}
Save
Abstract
En 中文
Efforts to understand autoimmunity have been pursued relentlessly for several decades. It has become apparent that the immune system evolved multiple mechanisms for controlling self-reactivity, and defects in one or more of these mechanisms can lead to a breakdown of tolerance. Among the multitude of lesions associated with disease, the most common seem to affect peripheral tolerance rather than central tolerance. The initial trigger for both systemic autoimmune disorders and organ-specific autoimmune disorders probably involves the recognition of self or foreign molecules, especially nucleic acids, by innate sensors. Such recognition, in turn, triggers inflammatory responses and the engagement of previously quiescent autoreactive T cells and B cells. Here we summarize the most prominent autoimmune pathways and identify key issues that require resolution for full understanding of pathogenic autoimmunity.
Keywords:
REGULATORY T-CELLS
PLASMACYTOID DENDRITIC CELLS
ARYL-HYDROCARBON RECEPTOR
LONG NONCODING RNA
CHAIN FATTY-ACIDS
I INTERFERON
B-CELLS
NUCLEIC-ACID
MOLECULAR MIMICRY
X-INACTIVATION
AI Summary
Key information extracted from the uploaded paper, including a brief overview, abstract, background, key highlights, visual analysis, and future outlook.