Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0039483 (giant cell arteritis)
 3,204 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An 80-year-old Japanese woman with temporal arteritis was treated with systemic recombinant human interleukin-2 (IL-2) (1 x 10(6) unit/day for six weeks). The presenting symptoms of headache and skin necrosis and abnormal laboratory findings, such as an elevated erythrocyte sedimentation rate and CRP, promptly improved without any serious side effects. Although the pathogenesis of temporal arteritis and the mechanism(s) of the beneficial effect of IL-2 on it still remain unknown, this preliminary study highly encourages further investigations.
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PMID:A case of temporal arteritis successfully treated with recombinant interleukin-2. 262 56

The original descriptions of polymyalgia rheumatica (PMR) and giant cell arteritis (GCA) in the medical literature date back to 1888 and 1890, respectively. Classification criteria for PMR and GCA are not standardized since most authors used subjective criteria based on their personal experience. Only one study has evaluated criteria for PMR and has found seven variables with high discriminant value. Criteria for GCA are less varied because a positive biopsy of the temporal artery is diagnostic. However, combinations of different clinical and laboratory features have been used for diagnosis when biopsy is negative or missing. Assessment of PMR/GCA is based on the serial determination of markers of acute phase such as ESR, CRP, or plasma viscosity. However, their value in predicting recurrence of the diseases is poor. New immunological factors including soluble interleukin-2 receptors, interleukin-6, serum soluble CD8, and serum soluble intercellular adhesion molecule-1 are presently under investigation.
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PMID:Polymyalgia rheumatica and giant cell arteritis. 749 36

Fourteen monoclonal antibodies were used to immunohistochemically label 22 temporal artery biopsy specimens taken from patients with temporal arteritis before treatment (n = 10), after 1.3 days of corticotherapy (n = 6) and after 12-30 days of steroids (n = 6). Histological sections from untreated patients revealed an inflammatory infiltrate comprised of approximately equal proportions of macrophages and T lymphocytes; the majority of the latter belonged to the CD4+ subset (the CD4+/CD8+ ratio varied from 2/1 to 4/1, depending upon the biopsy). These cells expressed high levels of HLA DR and low levels of interleukin-2 (IL2) receptors. A few B lymphocytes and plasmocytes were seen, mainly in the adventitia. Antigen-presenting cells (APC) were always found in the damaged media and natural killer cells (few in number) were sometimes present. Some macrophages were positively immunolabeled for IL6. A short, 1-to-3-day course of corticosteroids did not appreciably modify the lesions: cells remained highly activated, APC were seen in half the biopsies and IL6 immunolabeling persisted. The findings were essentially the same in treated but poorly controlled patients. Biopsies from 2 patients in clinical and biological remission revealed the persistence of an active immunological process. These observations indicate that the immunological process is poorly controlled by corticosteroid therapy.
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PMID:[Immunohistochemical study of lesions of temporal arteritis in Horton's disease]. 833 65

The Gfi-1 proto-oncogene encodes a zinc finger protein with six C2H2-type, C-terminal zinc finger motifs and is activated by provirus integration in T-cell lymphoma lines selected for interleukin-2 independence in culture and in primary retrovirus-induced thymomas. Gfi-1 expression in adult animals is restricted to the thymus, spleen, and testis and is enhanced in mitogen-stimulated splenocytes. In this report, we show that Gfi-1 is a 55-kDa nuclear protein that binds DNA in a sequence-specific manner. The Gfi-1 binding site, TAAATCAC(A/T)GCA, was defined via random oligonucleotide selection utilizing a bacterially expressed glutathione S-transferase-Gfi-1 fusion protein. Binding to this site was confirmed by electrophoretic mobility shift assays and DNase I footprinting. Methylation interference analysis and electrophoretic mobility shift assays with mutant oliginucleotides defined the relative importance of specific bases at the consensus binding site. Deletion of individual zinc fingers demonstrated that only zinc fingers 3, 4, and 5 are required for sequence-specific DNA binding. Potential Gfi-1 binding sites were detected in a large number of eukaryotic promoter-enhancers, including the enhancers of several proto-oncogenes and cytokine genes and the enhancer of the human cytomegalovirus (HCMV) major immediate-early promoter, which contains two such sites. HCMV major immediate-early-chloramphenicol acetyltransferase reporter constructs, transfected into NIH 3T3 fibroblasts, were repressed by Gfi-1, and the repression was abrogated by mutation of critical residues in the two Gfi-1 binding sites. These results suggest that Gfi-1 may play a role in HCMV biology and may contribute to oncogenesis and T-cell activation by repressing the expression of genes that inhibit these processes.
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PMID:Gfi-1 encodes a nuclear zinc finger protein that binds DNA and functions as a transcriptional repressor. 875