Induction of Anti-glomerular Basement Membrane (GBM) Nephritis*

We examined the capacity of mouse glomerular me-sangial cells (MC) to express and function through two different low affinity FcRs, the activating FcRIII and the inhibitory FcRII. Immunohistochemistry identi-fied FcRII as the prominent FcR in the kidney, and low levels of FcRIIb2-specific mRNA were also detected in primary cultures of growth-arrested MC. Activation by tumor necrosis factor-/interleukin-1 induced sub-stantial FcRII expression in proliferating MC. Impor-tantly, however, stimulation with interferon- (IFN-)/ lipopolysaccharide or IFN- alone resulted in a complete down-regulation of FcRII, which was accom-panied by a strong increase in FcR chain mRNA and a surface appearance of FcRIII. Activating FcRIII trig-gered mRNA synthesis for monocyte chemoattractan