Compartmentalization of Peyer's patch anlagen before lymphocyte entry (original) (raw)
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Journal of Experimental Medicine, 2000
Alymphoplasia (aly) mice, which carry a point mutation in the nuclear factor κB–inducing kinase (NIK) gene, are characterized by the systemic absence of lymph nodes and Peyer's patches, disorganized splenic and thymic architectures, and immunodeficiency. Another unique feature of aly/aly mice is that their peritoneal cavity contains more B1 cells than normal and aly/+ mice. Transfer experiments of peritoneal lymphocytes from aly/aly mice into recombination activating gene (RAG)-2−/− mice revealed that B and T cells fail to migrate to other lymphoid tissues, particularly to the gut-associated lymphatic tissue system. In vivo homing defects of aly/aly peritoneal cells correlated with reduction of their in vitro chemotactic responses to secondary lymphoid tissue chemokine (SLC) and B lymphocyte chemoattractant (BLC). The migration defect of aly/aly lymphocytes was not due to a lack of expression of chemokines and their receptors, but rather to impaired signal transduction downstrea...
Nephron, 1999
To clarify which matrix component(s) contributes to glomerular sclerosis with mesangial IgA deposits in a murine high serum IgA strain (HIGA) derived from ddY mice, morphological and immunopathological analyses of glomeruli were performed in comparison with original ddY and BALB/c mice as controls. Significantly increased thickness of the glomerular basement membrane (GBM), especially the lamina densa, was observed in HIGA mice. Immunofluorescent staining showed marked increases in levels of fibronectin and laminin in both the mesangium and capillary wall in aged HIGA mice. Analysis of the distribution of immunogold-labeled antibody in GBM revealed a significant increase (p < 0.0001) and specific orientation of fibronectin in the endothelial side, which suggested that mesangial fibronectin produced at high levels due to IgA deposition extended to the endothelial side of GBM and contributed to the thickening of GBM with further development to glomerulosclerosis in the HIGA mice.