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This chapter focuses on current advances in understanding of these immunocompetent cells and their role in experimental models of nephritis and human disease.
After intravenous administration of R-Gel labeled by Cy7 of a fluorescent dye to three animal models of nephritis mousse, interstitial nephritis (by using UUO model mice), glomerulonephritis (HIGA mice), and ischemia reperfusion injured kidney (I/R mice), the extent of fluorescent imaging at the renal inflammation was assessed.
Interestingly, experimental studies suggest that imatinib may improve animal models of nephritis like lupus and cryoglobulinaemia associated to membranoproliferative glomerulonephritis [ 7, 8].
In contrast, data also indicate that HSPGs may be anti-inflammatory, for example in disease models of nephritis and lung inflammation using sdc-1 and sdc-4 knockout mice [ 20- 25].
Infiltration of DCs in the glomeruli and tubulointerstitial spaces of the kidneys has been reported in various murine models of nephritis, including NZB/W F1 [ 67], anti-glomerular basement membrane (anti-GBM) [ 71], and mice engineered to express a foreign antigen on podocytes [ 66].
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Our finding that CCL3 inhibition enhances pathology is similar to the finding that in a model of nephritis CCR1−/− (the main receptor for CCL3) mice have enhanced pathology associated with increased TNF levels [16].
They considered the observed relation in line with the observations made in the passive Heymann model of nephritis, where proteinuria persisted after the decline in antibody titer, also supporting a pathogenic role for PLA2R ABs: the immunological phase of MN must end before a clinical response is to be seen.
We used our own data (presented here) and previously published data on the efficacy of mTOR inhibitors in two mouse models of lupus nephritis to infer that perturbations of the mTOR pathway are critical to the development of lupus nephritis in both these models.
Here we discuss the mouse models of lupus nephritis, C3 glomerulopathy and atypical hemolytic uremic syndrome, together with an inducible model of antiphospholipid syndrome.
There are at least four mouse models of lupus nephritis [ 14].
In experimental models of lupus nephritis, TNFα may play an immunosuppressive role at early stages of the disease.
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