Dnaso 1 |
SLE and scleroderma |
Macrophages and dendritic cells |
Mutation ot Dnase I is related to SLE and Scleroderma Dnasc I treatment prevents autmnunuiutv in mice |
58,
60,
61
|
Dnasc II |
Rheumatoid arthritis |
Macrophages |
Dnase II and IFNα double knockout mice develop age-dependent rheumatoid arthritis |
49,
50,
51,
55
|
TREX1 |
Aicaidi–Goutieres syndromes and SLE |
Macrophages |
Mutations in TREX1 gene were found in SLE patients. Loss of function mutation of TREX1 causes Aicardi–Goutieres syndromes TREX1 null mice develop inflammatory myocarditis with ssDNA accumulating in the cytoplasm |
53,
54
|
cGAS |
Aicanli–Goutieres syndromes, SLE Arthritis and SAVI (STING associated vasculopathy with onset in infancy) |
|
Gain-of-function mutations of the gene encoding STING in hunun patients with early-onset vasculopathy and pulmonary inflammationDeletion of cGAS rescues the Dnase II-deficient mice lacking functional TREX1 or RNaseH2, activation of the cGAS-STING pathway causes the Aicardi–Goutieres syndromes |
15,
22,
23
|
TLR9 |
SLE |
pDC and B cells |
TLR9 piomoted the B cells autoreactivity after chromatin engulfment.TLR9 mediated the type-1 IFN production after DNA immune complex uptake by pDC |
21,
101
|
DAI |
SLE |
Macrophages and dendritic cells |
DAI expression is upregulated in some SLE patients and one lupus mouse model.Apoptotic DNA immunization activated macrophages via DAI and DAI inhibition ameliorated SLE syndrome. |
24
|
AIM2 |
Psoriasis, SLE and inflammatory bowel disease |
Keratinocytes, macrophages |
AIM2 expression is upregulated in keratinocytes in promote IL-1 release. Cytosolic DNA promote IL-1 release from keratinocytes via AIM2.AMI2 expression is elevated in male SLE patients and inflammatory bowel disease |
25
|