Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immune complex glomerulonephritis was induced in three groups of mice by long-term immunization. Two antigens of similar molecular weight were used. The first group was immunized with ferritin (mol wt 480,000). In altered glomeruli deposits of immune complexes were seen in the subendothelial and subepithelial spaces of the glomerular basement membrane (GBM) and in the mesangium. The immune complex deposits were formed by amorphous matrix with marked dense molecules of ferritin. The second group was immunized with human fibrinogen (mol wt 450,000). The immune complex deposits were present in the intramembranous, subepithelial and subendothelial spaces of the GBM and in the mesangium. These deposits were relatively less electron-dense and had a fine granular structure. The third group of mice were immunized with both ferritin and fibrinogen simultaneously. Two types of deposits situated subendothelially in the GBM and in the mesangium were seen in one animal of this group. One type of deposit resembled structurally the ferritin-antiferritin complex deposits, the other resembled the fibrinogen-antifibrinogen complex deposits. The individual deposits in the GBM and in the mesangium formed discrete homogeneous masses. The two types of deposit were occassionally in direct contact with one another, but were more often completely separate and were never mixed. It can be assumed that in at least some phase of the experiment both types of complex were present in the circulating blood simultaneously. However, since none of the complexes deposited in the GBM or in the mesangium were mixed, it seems probable that each type of complex is deposited separately in the form of "clusters" composed of a single type of complex. The phagocytic activity of mesangial cells of animals with complex glomerulonephritis was not increased when compared with control animals.
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PMID:Experimental immune complex glomerulonephritis in the mouse with two types of immune complexes. 14 86

Immune complex glomerulonephritis (GN) often deteriorates during infection with viruses and bacteria that, in contrast to mammals, have DNA that contains many unmethylated CpG motifs. Balb/c mice with horse apoferritin-induced GN (HAF-GN) were treated with either saline, CpG-oligodeoxynucleotides (ODN), or control GpC-ODN. Only CpG-ODN exacerbated HAF-GN with an increase of glomerular macrophages, which was associated with massive albuminuria and increased renal MCP-1/CCL2, RANTES/CCL5, CCR1, CCR2, and CCR5 mRNA expression. CpG-ODN induced a Th1 response as indicated by serum anti-HAF IgG(2a) titers, mesangial IgG(2a) deposits, and splenocyte IFN-gamma secretion. Messenger RNA for the CpG-DNA receptor Toll-like reeptor 9 (TLR9) was present in kidneys with HAF-GN but not in normal kidneys. The source of TLR9 mRNA in HAF-GN could be infiltrating macrophages or intrinsic renal cells, e.g., mesangial cells; but, in vitro, only murine J774 macrophages expressed TLR9. In J774 cells, CpG-ODN induced the chemokines MCP-1/CCL2 and RANTES/CCL5 and the chemokine receptors CCR1 and CCR5. It is concluded that CpG-DNA can aggravate preexisting GN via a shift toward a Th1 response but also by a novel pathway involving TLR9-mediated chemokine and chemokine receptor expression by macrophages, which may contribute to the enhanced glomerular macrophage recruitment and activation. This mechanism may be relevant during infection-triggered exacerbation of human immune-complex GN and other immune-mediated diseases in general.
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PMID:Bacterial CpG-DNA aggravates immune complex glomerulonephritis: role of TLR9-mediated expression of chemokines and chemokine receptors. 1253 32