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)

Injection of small amounts of ferritin intravenously, into the aorta (above the renal arteries) or into the left renal artery of rabbits hyperimmunized against this protein, results in the formation of circulating, insoluble, antigen-antibody complexes. Some of these complexes localize focally in the renal glomerular capillaries, where they elicit severe lesions. The fate of the complexes and the evolution of the lesions have been followed by immunofluorescent and electron microscopic techniques. Within a few hours, the deposition of complexes in the glomeruli resulted in a massive accumulation of neutrophils platelets, and fibrin, sometimes leading to acute focal necroses of some loops. These lesions were quite similar to those developing in the small dermal vessels during the Arthus reaction. Most of the complexes were rapidly phagocytosed and degraded by neutrophils; swelling and proliferation of endothelial and mesangial cells usually followed the acute damage and contributed to the removal of remaining complexes, cell debris, and fibrin deposits. Later, focal areas of mesangial proliferation and sclerosis were observed, containing large amounts of basement membrane-like material and sometimes of collagen fibrils; synechiae and crescent formation were noted in certain places. These observations suggest that the glomerular localization of very large, poorly soluble or insoluble immune complexes may be responsible for the focal glomerular changes seen in association with subacute bacterial endocarditis, with anaphylactoid purpura, or for some of the most severe lesions developing during chronic immune complex diseases.
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PMID:Experimental focal glomerular lesions elicited by insoluble immune complexes. Ultrastructural and immunofluorescent studies. 108 37

The effect of ferritin on the delayed-type hypersensitivity (DTH) response and Arthus-type reaction as assessed by footpad reaction using methylated human serum albumin, human serum albumin, or sheep red blood cells as antigens was investigated. Intraperitoneally administered ferritin was short acting and suppressed either induction or expression of DTH depending on the time of ferritin injection although it did not inhibit the antibody-mediated inflammatory response, the Arthus reaction. Investigation of ferritin's effect on the primary antibody response revealed that the number of IgG plaque-forming cells (PFC) was moderately decreased but IgM PFC were not. These results indicate that the afferent limb, ferritin selectively suppresses antigen presentation and/or clonal expansion of effector cells of cell-mediated immunity, but not that of the antibody response. Antigen presentation by Ia-positive cells and/or lymphokine-responsive inflammatory mononuclear cells at the efferent limb of DTH is suggested to be affected by ferritin. This conclusion is based upon the observations of successful TDTH effector cell transfer from sensitized but ferritin-treated donors and of successful reversal of ferritin-induced suppression of expression of DTH by supplementing normal bone marrow-derived cells containing Ia-positive ones. Thus our in vivo experimental system might be useful for the differential analysis of immunopathological lesions such as a T-cell-mediated, monocyte-dependent and an antibody-mediated inflammatory lesions.
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PMID:Ferritin selectively suppresses delayed-type hypersensitivity responses at induction or effector phase. 295 43

Experimental arthritis was induced in rats by the use of horse ferritin as an antigen. The pathological findings were studied and the mechanisms of inflammation were analyzed. Arthritis was induced through various mode of actions: 1. Arthus reaction (antigen-induced arthritis). 2. Passive Arthus reaction. 3. Reverse passive Arthus reaction. 4. Arthritis induced by intra-articular injection of immune complex, by either single shot or repeated injections. 5. Arthritis induced by anamnestic reaction. Arthritis induced by repeated injections of immune complex or that induced by anamnestic reaction exhibited mild chronic synovitis characterized by round cell infiltration without detectable acute phase of inflammation. Arthritis induced through other immunological mechanisms revealed a sequential course of acute synovitis characterized by accumulation of polymorphonuclear leucocytes (PMN) followed by gradual disappearance of PMN and alternative increase of round cells or plasma cells and proliferation of synovial lining cells. All types of arthritis subsided with mild fibrosis of the synovial tissue without lasting over a significantly long time. Although the successful production of a long-lasting chronic arthritis has been reported in rabbits, it was impossible to induce such long standing arthritis through this experiment. The chronicity of the arthritis induced through immunological mechanism may not simply be due to the long-standing retention of immune complex within the involved joint but also due to other factors such as the species of the test animals, the nature of antigen used and local factors produced through acute joint inflammation.
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PMID:[Comparative study on rat arthritis induced by various immune mechanisms (author's transl)]. 645 55