<b>Results:</b> Hepatic accumulation of <sup>18</sup>F-FDG and <sup>18</sup>F-FAC was 173% and 61% higher, respectively, and hepatic accumulation of <sup>18</sup>F-DFA was 41% lower, in a mouse model of autoimmune hepatitis than in control mice.
In conclusion, bone marrow stem cell derived exosomes can protect liver injury in an experimental model of autoimmune hepatitis and the mechanism could be related to exosomal miR-223 regulation of NLRP3 and caspase-1.
These finding indicate that O-GlcNAc glycosylation plays a critical role in the activation of Notch signaling, which could promote Treg differentiation in the liver to inhibit T cell infiltration and control disease development in autoimmune hepatitis.
Collectively, our data indicate that the Nrf2/HO-1/CO pathway is fundamental for the regulation of the immune responses, and that therapeutic intervention aimed at its modulation by CORM-A1 may represent a valuable strategy to be considered for the treatment of autoimmune hepatitis in humans.
Our comprehensive evaluation of various classical and novel autoantibody biomarkers including Ro52/TRIM21, anti-p53, anti-KLHL-12 and anti-HK-1 were not significantly associated with PBC-AIH OS.
Our comprehensive evaluation of various classical and novel autoantibody biomarkers including Ro52/TRIM21, anti-p53, anti-KLHL-12 and anti-HK-1 were not significantly associated with PBC-AIH OS.
Also, the serum levels of IL-17A and IL-22 were correlated positively with liver injury (ALT/AST), whereas the serum levels of IL-10 were correlated negatively with hypergammaglobulinaemia (IgG, IgM) in AIH patients.
In conclusion, our results highlight NKG2D as an essential receptor required for the activation of iNKT cells in Con A-induced hepatitis and indicate that it represents a potential drug target for prevention of autoimmune hepatitis.
The present study indicated that L-THP attenuated acute liver injury in ConA-induced autoimmune hepatitis by inhibiting apoptosis and autophagy via the TRAF6/JNK pathway.
Here we report that the amplified non-AIH liver inflammation could promote the initiation of AIH due to the sustained increase of IL-6, IL-12, IL-4, and IL-25 in the liver.
This is the first report of simultaneous strong accumulation of FDG and Glut-3 expression in IgG4-related AIH, which might aid in elucidating the pathogenesis of this disease.
However, GLP-1 mimetic medicines have reported clinical side effects, such as autoimmune hepatitis, acute kidney injury, pancreatitis, and pancreatic cancer.
More importantly, for the first time we found that patients with DIAIH had higher levels of serum ALT and AST, more severe degree of lobular inflammation, higher frequencies of zone 3 necrosis and higher number of lobular CD4<sup>+</sup>Foxp3<sup>+</sup>CD25<sup>-</sup>Tregs compared with AIH (P < 0.05).
The present study indicated that L-THP attenuated acute liver injury in ConA-induced autoimmune hepatitis by inhibiting apoptosis and autophagy via the TRAF6/JNK pathway.
Our data demonstrated that antagomir-155 treatment could prevent AIH via regulating the differentiation of Treg and Th17 cells, suggesting that microRNA-155 may be an intriguing therapeutic target of AIH.
<b>Results:</b> Hepatic accumulation of <sup>18</sup>F-FDG and <sup>18</sup>F-FAC was 173% and 61% higher, respectively, and hepatic accumulation of <sup>18</sup>F-DFA was 41% lower, in a mouse model of autoimmune hepatitis than in control mice.
In conclusion, our results highlight NKG2D as an essential receptor required for the activation of iNKT cells in Con A-induced hepatitis and indicate that it represents a potential drug target for prevention of autoimmune hepatitis.