Inflamed kidneys of NZB/W mice are a major site for the homeostasis of plasma cells

(NZB x NZW)F1 (NZB/W) mice develop a disease similar to human systemic lupu s erythematosus (SLE), including autoantibody production, hypergammaglobuli naemia and inflammation of the kidneys. It is known that large numbers of l ymphocytes infiltrate the kidneys of these mice. Here, we compare the roles of bone marrow, spleen and inflamed kidneys of NZB/W mice in the activatio n of B cells and the persistence of antibody-secreting cells (ASC). ASC are present in the kidneys of NZB/W mice with full-blown disease, as many as i n the spleen and bone marrow. The specificity of the ASC in the inflamed ki dneys is not restricted to self-antigens. After immunization of NZB/W mice with ovalbumin (OVA) the OVA-specific ASC are found initially in the spleen . Weeks later, OVA-specific ASC are found in high numbers in the bone marro w and the kidneys of these mice, but no longer in the spleen. As determined by FACS, B cells with a germinal center phenotype (B220(+)/PNA(+)) are fou nd only in very low numbers in the kidneys, but in high numbers in the sple en of NZB/W mice. Germinal centers could not be detected in the kidneys, bu t in-the spleen, and plasma cells appear to be scattered over the tissue. T hese data suggest that in autoimmune NZB/W mice, plasma cells generated in immune reactions of secondary lymphoid organs, later accumulate and persist in the inflamed kidneys, were they enhance the local concentrations of Ab and immunocomplexes. These experiments identify the inflamed kidneys of NZB /W mice as a site of prime relevance for the homeostasis of plasma cells, i rrespective of their specificity.