Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Granulomatous inflammatory lesions are a major histopathological feature of a wide spectrum of human infectious and autoimmune diseases. Experimental autoimmune thyroiditis (EAT) with granulomatous histopathological features can be induced by mouse thyroglobulin (MTg)-sensitized spleen cells activated in vitro with MTg and anti-interleukin-2 receptor (anti-IL-2R), anti-IL-2, or anti-interferon-gamma (anti-IFN-gamma) monoclonal antibody (MAb). These studies suggested that IFN-gamma-producing T cells requiring IL-2 for growth may negatively regulate activation of granulomatous EAT effector cells. As IL-12 promotes activation of IFN-gamma-producing Th1 cells, the present study was undertaken to determine the role of IL-12 in activation of effector cells for granulomatous EAT. MTg-sensitized cells activated in vitro with MTg, anti-IL2R MAb, and IL-12 induced severe, destructive granulomatous thyroiditis with neutrophil inflammation, fibrin deposition, and necrosis. Many glands ultimately underwent atrophy and became fibrotic; some also showed fibrinoid necrosis and a mixed inflammatory cell infiltration of blood vessel walls indicative of a necrotizing vasculitis. Induction of severe granulomatous EAT by IL-12 required MTg in vitro and was unrelated to the IL-12-induced increase in IFN-gamma production. IL-12 markedly increased IFN-gamma production but did not induce a shift to a Th1-dominant phenotype, as other Th1 and Th2 cytokines were generally unaffected and both Th1 and Th2 cytokines were expressed in recipient thyroids. Addition of IL-12 or neutralization by anti-IL-12 at various times indicated that IL-12 exerted its primary effects in the final 24 hours of the 72-hour culture and was not required in recipient mice. Cells cultured with anti-IL-12, MTg, and anti-IL2R MAb transferred mild lymphocytic EAT but little or no granulomatous EAT. Thus, IL-12 profoundly regulates the in vitro activation of effector cells that induce histologically distinct autoimmune inflammatory lesions in the thyroid.
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PMID:Interleukin-12 promotes activation of effector cells that induce a severe destructive granulomatous form of murine experimental autoimmune thyroiditis. 958 3

A 66-year-old man who had been given a clinical diagnosis of vasculitis at another hospital after presenting with high fever and rash was admitted to our hospital for further examination following a relapse of fever during steroid reduction. The biopsy specimens of the leg with crusts showed the presence of epithelioid granuloma, and because of a negative tuberculin test, increased serum angiotensin converting enzyme (ACE) and lysozyme levels, and pulmonary Ga uptake, the patient was given a diagnosis of sarcoidosis. Although the patient had been treated on an outpatient basis following resolution of fever with NSAIDs and 5 mg prednisolone (PSL), he suffered acute respiratory failure during follow-up and required emergency admission. Chest CT revealed bilateral ground-glass opacity and pleural effusion, and serum ACE and soluble IL2R levels were significantly elevated. We diagnosed acute exacerbation of sarcoidosis and given high dose steroid therapy. The patient's symptoms, image findings, blood test results, and other findings promptly improved. Here we reported a highly unusual presentation of acute respiratory failure in sarcoidosis.
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PMID:[A case of sarcoidosis presenting with high fever and rash progressing to acute respiratory failure]. 1792 71