kn-93 and nephrin

We have found that calcium calmodulin kinase IV is increased in T cells, podocytes, and mesangial cells from patients with systemic lupus erythematosus, as well as in lupus-prone mice, podocytes of patients with focal segmental glomerulosclerosis, and in mice injected with doxorubicin. We showed that this accounts for aberrant T cell function and glomerular damage. Using nanoparticles (nlg) loaded with a small drug inhibitor of calcium calmodulin kinase IV and tagged with antibodies directed to CD4 we have been able to show inhibition of autoimmunity and lupus nephritis. Also, using nlg tagged with antibodies to nephrin, we showed suppression of nephritis in lupus-prone mice and of glomerular damage in mice exposed to doxorubicin. We propose the development of approaches to deliver drugs to cells in a targeted and precise manner.

Topics: Animals; Antibiotics, Antineoplastic; Benzylamines; Calcium-Calmodulin-Dependent Protein Kinase Type 4; CD4 Antigens; Disease Models, Animal; DNA Methylation; Doxorubicin; Drug Delivery Systems; Glomerulosclerosis, Focal Segmental; Humans; Lupus Erythematosus, Systemic; Lupus Nephritis; Membrane Proteins; Mice; Mice, Inbred MRL lpr; Molecular Targeted Therapy; Nanoparticles; Protein Kinase Inhibitors; Sulfonamides; T-Lymphocytes; T-Lymphocytes, Regulatory; Th17 Cells