the disease substantially reduced proteinuria, prevented effects compared with glucocorticoids, they do not have any increased efficacy.It is in this area where the loss of renal function, significantly reduced histological damage including glomerular crescent forma-anti-MIF treatment could prove to have significant advantages over other anti-inflammatory drugs.MIF tion, and substantially inhibited renal leucocytic infiltration and activation [9].Further examination can overcome glucocorticoid-mediated inhibition of cytokine production [5], therefore high levels of MIF showed that anti-MIF mAb treatment prevented the marked up-regulation of IL-1b, ICAM-1, VCAM-1 may be a crucial factor limiting the immunosuppressive effects of even high-dose glucocorticoid treatment.The and iNOS expression seen in the control antibodytreated animals.Anti-MIF mAb treatment suppressed next key step in developing anti-MIF therapy is to determine whether the combination of anti-MIF mAb a skin DTH response to the immunizing antigen, but failed to inhibit the secondary humoral response.plus glucocorticoid treatment can provide a greater degree of disease suppression compared with either Having established the pathological importance of MIF in the induction and development of experimental agent alone.If this proves to be the case, then a combination of anti-MIF treatment plus low-dose crescentic glomerulonephritis, we examined whether anti-MIF mAb treatment could halt or even reverse glucocorticoids could become the treatment of choice for many types of kidney disease, and indeed immuno-established crescentic disease [10].To do this, anti-MIF mAb treatment was delayed until day 7, at which logical diseases generally.time renal impairment and crescent formation were evident.Compared with animals examined on day 7, treatment with the irrelevant control mAb over days 7-21 led to a rapidly progressive glomerulonephritis with severe renal injury (proteinuria), loss of renal 1. Hooke DH, Gee DC, Atkins RC.Leukocyte analysis using formation).In contrast, anti-MIF mAb treatment over monoclonal antibodies in human glomerulonephritis.Kidney Int days 7-21 partially reversed the disease by restoring 1987; 31: 964-972 2. Calandra T, Bucala R. Macrophage migration inhibitory factor normal renal function and reducing histological (MIF ): a glucocorticoid counter-regulator within the immune damage compared with untreated animals examined system.
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