We report that passive transfer of human SLE sera into mice expressing the uniquely human FcγRIIA and FcγRIIIB on neutrophils induces lupus nephritis and in some cases arthritis only when the mice additionally lack the CD18 integrin, Mac-1.
Taken together, our findings suggest that Fkn and CD16(+) Mo accumulation are partially associated with the severity and diversity of histology of lupus nephritis.
We then examined CNV at FCGR3B in relation to SLE and SLE nephritis within a case-control collection of 134 cases of SLE (37 with SLE nephritis) and 589 population controls of mainly Afro-Caribbean descent resident in Trinidad.
SLE patients with lupus nephritis were also associated with higher levels of circulating CD16- monocytes and total monocytes, in comparison with that of controls (both p < 0.0001).
Lupus nephritis (OR = 2.84; 95%CI 1.14-7.03, P = 0.02) and the presence of anti-Sm antibodies (OR = 3.11; 95%CI 1.08-8.94; P = 0.03) were significantly more prevalent among lupus patients possessing the TNF-308 A allele.
OTUB1 overexpression was detected in the mesangial area of glomeruli in some immunocomplex mediated nephritides such as IgA nephropathy, acute diffuse proliferative glomerulonephritis and lupus nephritis by immunohistochemistry.
The glomerular number of 400 mg/kg treated mice was more than control group.Treatment with 400 mg/kg <i>D. candidum</i> reduced IL-6, IL-12, TNF-α and IFN-γcytokine levels as compared to control mice.<i>D. candidum</i> decreased NF-κb, TGF 'β1, Fas, FasL and increased IκB-α expressions in kidney tissue.There were 11 compounds in dry <i>D. candidum</i>, these compounds might make the curative effects of lupus nephritis.
The levels of retinoic acid-related orphan receptor c and IL-17 mRNA are significantly higher in PBMCs from children with LN than in those from controls.
The data show that baicalein alleviates the symptoms of pristane-induced LN and suggest that the alleviation may be attributed to inhibition of MDSC expansion and regulation of the balance of the Nrf2/HO-1 signal and NLRP3 expression in MDSCs.
Uncontrolled studies in patients with treatment-refractory lupus nephritis showed a significant reduction in proteinuria with ACE-inhibitors and Angiotensin receptor blockers treatment.
MiR-125a-3p could be a important factor in the pathogenesis of LN which causes decrease in expression of IL-17 by potentially binding to the 3'UTR region causing suppression of fibrosis via down-regulating TGF-β1 in the SV40MES13 rat mesangial cells.