Dense deposit disease (DDD), known as type II MPGN, is an uncommon form of glomerulonephritis. It is an acquired primary glomerular disease, characterised by electron microscopic evidence of a continous, dense membrane deposition replacing the lamina densa. There is associated alternative pathway complement activation and a C3 nephritic factor maybe present. Patients with dense deposit disease tend to be young at clincal onset and more commonly have persistent nephrotic syndrome, gross hematuria, and acute nephritis episode and persistent depression of the serum complement level. The prognosis of dense deposit disease is worse than that of type I MPGN. We experienced a patient with dense deposit disease that presenting persistent nephrotic syndrome, gross hematuria and having subepithelial hump. It is a first report of dense deposit disease having subepithelial hump in Korea, therefore we report this case with the review of relevant literatures.
Head and neck squamous cell carcinoma(HNSCC) has been associated with host immunosuppression, including depressed T-lymphocyte and natural killer cell function. This immunosuppression has been shown to be most pronounced in the locoregional environment of the tumor and appears to be mediated by soluble suppressor factor prostaglandinE2(PGE2). PGE2 is a product of cell membrane phospholipid metabolism that is known to have potent immunoregulatory activity including inhibition of natural killer cell activity and antibody dependent cell mediated cytotoxicity(ADCC).
In our experiment, we have established an ADCC assay with IgGl cMAB SF-25, 323A/3 using human squamous cell carcinoma of the head and neck cell line(PCI-50) as target. The measurement of cytotoxicity was determined by measuring the release of 51Chromium from the target cells after 4 hour incubation.
PGE2 inhibited antibody dependant cell mediated cytotoxicity.
It thus implies that the production of prostaglandins by tumor cells may constitute a means by which the tumor cells subvert the effect of a cellular immune response that is directed against them and arming of NK cells with chimeric antibody could be considered in developing means for treatment of human SCCHN in adjuvant setting.