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)

The natural killer cell activity (NKCA) of a population of 66 functioning kidney allograft recipients (followed up for over 9 years) was assessed on K562 and DORA cell line targets. The 51Cr specific release test showed a rapid, sharp decrease in NKCA as early as 3 months after grafting, reaching a minimal level between 7 and 60 months (5 +/- 5 vs. 45 +/- 19% 51Cr release; P less than 0.001). Patients showing an almost total lack of NKCA were roughly the same whether assessed on K562 or DORA targets. NKCA tended to be restored in long-term transplanted patients (greater than 61 months). Control populations, aside from 32 healthy individuals, consisted of 11 haemodialysed patients as well as patients submitted to corticosteroid therapy for more than one year (8 cases of giant cell arteritis and 4 chronic asthmas). Haemodialysed patients exhibited normal NKCA (whether previously grafted or not). Corticosteroid-treated patients showed either no significant modification (K562 target) or a borderline decrease (DORA target) in NKCA. Azathioprine or corticosteroid dosage intake on the day of the test did not influence the level of graft recipient NKCA. The natural cytotoxicity of peripheral blood lymphocytes (PBL) from recipients lacking in activity (less than 5% 51Cr release) was not restored by exogenous (type alpha) interferon. and PBL of recipients with low NKCA scores produced normal levels of purified interferon after 24-h Sendai virus exposure. No inhibitory effects of sera obtained from recipients lacking NKCA nor any active suppressor cells from their PBL could be evidenced, thus suggesting an actual loss of natural killer progenitors (or an "insensitivity" to interferon) in those patients. Corticosteroids, as opposed to azathioprine, were able to decrease the in vitro NKCA of healthy donor PBL at pharmacological concentrations.
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PMID:Decrease in natural killer cell activity in kidney allograft recipients. 619 19

Peripheral blood lymphocytes from 23 patients with polymyalgia rheumatica (PMR) were characterized using monoclonal antibodies and flow cytometry in a two-year prospective study. There were no significant differences in absolute numbers or relative percentages of lymphocytes or CD3+, CD4+, CD8+ T cells or the CD4+ T cell functional subsets, virgin (CD4+CD45RA+) and memory (CD4+CD29+) T cells, in patients before or during corticosteroid treatment compared to controls. Previous reports on decreased levels of CD8+ T cells as a characteristic of PMR/giant cell arteritis was not confirmed. The absolute number and relative percentage of lymphocytes with natural killer cell activity, CD16+ CD56+ cells, were significantly lower in patients with active untreated PMR as well as during corticosteroid treatment compared to controls, but at the two-year follow-up the difference was less marked.
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PMID:Peripheral blood lymphocyte subsets in polymyalgia rheumatica. 774 46

The Fc gamma receptors have been shown to play important roles in the initiation and regulation of many immunological and inflammatory processes and to amplify and refine the immune response to an infection. We have investigated the hypothesis that polymorphism within the FCGR genetic locus is associated with giant cell arteritis (GCA). Biallelic polymorphisms in FCGR2A, FCGR3A, FCGR3B and FCGR2B were examined for association with biopsy-proven GCA (n = 85) and healthy ethnically matched controls (n = 132) in a well-characterised cohort from Lugo, Spain. Haplotype frequencies and linkage disequilibrium (D') were estimated across the FCGR locus and a model-free analysis performed to determine association with GCA. There was a significant association between FCGR2A-131RR homozygosity (odds ratio (OR) 2.10, 95% confidence interval (CI) 1.12 to 3.77, P = 0.02, compared with all others) and carriage of FCGR3A-158F (OR 3.09, 95% CI 1.10 to 8.64, P = 0.03, compared with non-carriers) with susceptibility to GCA. FCGR haplotypes were examined to refine the extent of the association. The haplotype showing the strongest association with GCA susceptibility was the FCGR2A-FCGR3A 131R-158F haplotype (OR 2.84, P = 0.01 for homozygotes compared with all others). There was evidence of a multiplicative joint effect between homozygosity for FCGR2A-131R and HLA-DRB1*04 positivity, consistent with both of these two genetic factors contributing to the risk of disease. The risk of GCA in HLA-DRB1*04 positive individuals homozygous for the FCGR2A-131R allele is increased almost six-fold compared with those with other FCGR2A genotypes who are HLA-DRB1*04 negative. We have demonstrated that FCGR2A may contribute to the 'susceptibility' of GCA in this Spanish population. The increased association observed with a FCGR2A-FCGR3A haplotype suggests the presence of additional genetic polymorphisms in linkage disequilibrium with this haplotype that may contribute to disease susceptibility. These findings may ultimately provide new insights into disease pathogenesis.
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PMID:Association of FCGR2A and FCGR2A-FCGR3A haplotypes with susceptibility to giant cell arteritis. 1684 26