Serum sTyro3, sAxl, sMer, and Gas6 levels were measured using ELISA in 67 JSLE patients, 12 juvenile idiopathic arthritis (JIA) inflammatory and 20 healthy controls and related with SLEDAI-2K score, anti-dsDNA antibody, ESR, CRP, C3, C4 levels, and nephritis.
Nephritis-associated plasmin receptor (NAPlr) was originally isolated from group A streptococci as the protein responsible for acute poststreptococcal glomerulonephritis, and was shown to be identical to streptococcal glyceraldehyde-3-phosphate dehydrogenase (GAPDH).
Using a FACS-based protocol that allowed comparative analysis of cortical epithelial cell populations, we showed that particularly proximal tubular epithelial cells (PTECs) express molecules linked with antigen-presenting cell function, including major histocompatibility complex class II (MHCII), CD74, CD80, and CD86 in homeostasis and nephrotoxic nephritis, a murine model of cGN.
Overproduction of non-ecotropic ERV (NEERV) envelope glycoprotein gp70 and resultant nephritis occur in lupus-prone mice, but whether NEERV mis-expression contributes to lupus etiology is unclear.
Interfering with the interaction between biglycan and specific TLR co-receptors could represent a promising therapeutic intervention to curtail kidney inflammation and damage.
Compared with the control group, ILCs (Lin-CD127+CD45+ cells) were higher in SLE patients (p<0.01), and the distribution of ILC population changed between groups, ILC1 (Lin-CD127+CD45+CRTH2-CD117-cells)/ILC3 (Lin-CD127+CD45+CRTH2-CD-117+cells) count increased (p<0.0001) and correlated with nephritis and disease activity.
F1 crosses of lupus-prone New Zealand Black (NZB) and 129 mice to Snerv1/Snerv2<sup>-/-</sup> mice failed to restore NEERV repression, demonstrating that loss of SNERV underlies the lupus autoantigen gp70 overproduction that promotes nephritis in susceptible mice and that SNERV encodes for Sgp3 (in NZB mice) and Gv-1 loci (in 129 mice).
Overall, these data demonstrate that NAC could ameliorate cisplatin-induced nephrotoxicity in mice and the protective effects may be conducted by inhibiting the activation of kidney inflammation and the complement system.
Hyaluronic acid (HA), a component of the extracellular matrix, is the ligand for CD44 and has been implicated in the pathogenesis of kidney inflammation in patients with systemic lupus erythematosus (SLE), but its direct role and mechanism of action have not been studied.
Genetic Nlrp6 deficiency resulted in upregulation of kidney extracellular signal-regulated kinase 1/2 (ERK1/2) and p38 mitogen-activated protein kinase (MAPK) phosphorylation and more severe AKI and kidney inflammation.
Furthermore, anti-α-enolase Ab combined with β2-MG for evaluating the incidence of nephritis in SLE patients had the best assessment of the effectiveness (area under the receiver operating characteristic curve (AUC): 92.7%) compared with only anti-α-enolase Ab (AUC: 80.9%) or β2-MG (AUC: 84.5%).
We propose that better understanding of the role of IKK-2 and NEMO in nephritis is essential for the clinical application of kinase inhibitors in patients with glomerulonephritis.-Guo, L., Huang, J., Chen, M., Piotrowski, E., Song, N., Zahner, G., Paust, H.-J., Alawi, M., Geffers, R., Thaiss, F. T-lymphocyte-specific knockout of IKK-2 or NEMO induces T<sub>h</sub>17 cells in an experimental nephrotoxic nephritis mouse model.
Compared with the control group, ILCs (Lin-CD127+CD45+ cells) were higher in SLE patients (p<0.01), and the distribution of ILC population changed between groups, ILC1 (Lin-CD127+CD45+CRTH2-CD117-cells)/ILC3 (Lin-CD127+CD45+CRTH2-CD-117+cells) count increased (p<0.0001) and correlated with nephritis and disease activity.
Furthermore, patients with exogenous low-dose IL-2 supplement demonstrated better improved nephritis and higher remission rate (55.56%, P = 0.058) than those with conventional therapy.
Overproduction of non-ecotropic ERV (NEERV) envelope glycoprotein gp70 and resultant nephritis occur in lupus-prone mice, but whether NEERV mis-expression contributes to lupus etiology is unclear.