Person: DİRESKENELİ, RAFİ HANER
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DİRESKENELİ
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RAFİ HANER
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Publication Metadata only Behcet's disease in patients with chronic myelogenous leukemia: Possible role of interferon-alpha treatment in the occurrence of Behcet's symptoms(SPRINGER VERLAG, 1997) DİRESKENELİ, RAFİ HANER; BudakAlpdogan, T; Demircay, Z; Alpdogan, O; Direskeneli, H; Ergun, T; Bayik, M; Akoglu, TTwo patients with chronic myelogenous leukemia (CML) who developed characteristic features of Behcet's disease (ED) during alpha-interferon (IFN-alpha) treatment and another patient who had a diagnosis of ED preceding CML are presented. In the first two patients, features of ED appeared 6 months after the initiation of IFN-alpha treatment; they included recurrent oral aphthae, genital ulceration, arthritis, folliculitis, and a positive skin pathergy test. The third patient, however, had a diagnosis of Behcet's disease 4 years before diagnosis of Philadelphia-positive CML. We prospectively examined the skin pathergy reaction in a group of patients with CML, multiple myeloma, and hairy cell leukemia both before and after IFN-alpha treatment and found two additional patients with CML who developed a positive skin pathergy test following IFN-alpha treatment.Publication Metadata only Anti-lymphocyte, anti-monocyte, and anti-endothelial cell antibodies in chronic haemodialysis patients(1992) DİRESKENELİ, RAFİ HANER; Direskeneli H., Özgön S., Özener C., Lawrence R., Erman M., Sarsmaz N., Akoglu E.Patients receiving chronic haemodialysis treatment are known to have a high prevalence of anti-panel antibodies (anti-lymphocyte, antimonocyte, and anti-endothelial cell) originating from a number of different possible sensitizing events such as blood transfusions, multiparity, or renal transplantation. © 1992 European Dialysis and Transplant Association-European Renal Association.Publication Metadata only Recognition of B-Cell Epitopes of the 65 kDa HSP in Behçet's Disease(Blackwell Publishing Ltd., 1996) DİRESKENELİ, RAFİ HANER; Direskeneli H., Hasan A., Shinnick T., Mizushima Y., Van Der Zee R., Fortune F., Stanford M.R., Lehner T.B-cell epitopes of the mycobacterial 65 kDa heat shock protein (HSP) were mapped in sera from patients with Behçet's Disease (BD). A series of 47 overlapping synthetic peptides (15ers) derived from the sequence of the Mycobacterium tuberculosis 65 kDa HSP was used in ELISA. Significant increases in IgA and IgG antibody levels were observed with peptides 111-125, 154-172 and 311-326 in sera from BD, compared with those from controls. Homologous peptides derived from the sequence of the human mitochondrial 60 kDa HSP were then examined. Peptides 136-150 and 336-351 showed comparable results to the homologous mycobacterial peptides 111-125 and 311-326, respectively. The B-cell epitopes defined in this investigation overlap with the T-cell epitopes the authors have previously reported in BD. Inhibition studies are consistent with the view that antibodies to each of the three B-cell epitope peptides represent a small proportion of the total B-cell epitope repertoire elicited by the 65 or 60 kD HSP. Sequential antibody studies suggest that IgA and IgG antibody titres to one or all three peptides tested may increase during exacerbations of ocular disease. The functional role of these antibodies needs to be determined, but the peptides may be involved in the immunopathogenesis of BD as they can induce experimental uveitis in Lewis rats, which is a principal manifestation of BD.Publication Open Access Neutrophil adhesion to endothelial cells and factors affecting adhesion in patients with Behcet's disease(B M J PUBLISHING GROUP, 1996-02-01) DİRESKENELİ, RAFİ HANER; Sahin, S; Akoglu, T; Direskeneli, H; Sen, LS; Lawrence, RObjectives-To study the in vitro adhesion of polymorphonuclear leucocytes (PMNLs) to endothelial cells in patients with Behcet's disease (ED), and the humoral and cellular factors which may contribute to adhesion. Methods-A total of 118 patients with ED and 60 healthy controls were studied. In vitro adhesion of chromium-51 labelled normal neutrophils to human umbilical vascular endothelial cell (HUVEC) monolayers were studied in the presence of normal serum or serum obtained from patients with ED. Adhesion of neutrophils from patients with ED to HUVEC stimulated with tumour necrosis factor (TNF), interleukin-1 (IL-1), and lipopolysaccharide (LPS) and adhesion molecule (CD11a, CD11b, CD18 and L-selectin) expression on the patient's neutrophils and lymphocytes were determined, and the serum concentration of IL-8 was measured. Results-Sera from patients with ED were found to enhance the adherence of normal PMNLs to HUVEC monolayers in vitro. Patients' sera induced an increase in surface expression of CD11a and CD18 on normal neutrophils and intercellular adhesion molecule-1 (ICAM-1) expression on HUVECs. The number of CD11a positive neutrophils was greater in the blood of patients with ED than in that of healthy controls (89.4% v 71%; p < 0.001). Pretreatment of HUVECs with IL-1 alpha, TNF alpha or LPS resulted in an increased adhesion of patients' PMNLs greater than that observed for normal PMNLs. Monoclonal antibodies to CD11a, CD11b, CD18, and ICAM-1 caused varying degrees of inhibition of neutrophil adhesion. The concentration of IL-8 was also found to be significantly increased in sera of patients with ED (490 (SD 470) pg/ml) compared with normal controls (97.5 (56.3) pg/ml). Conclusion-Abnormalities of neutrophils, endothelial cells, or both, have been suggested to be responsible for many of the clinical manifestations of ED. Our findings may explain the underlying mechanism of neutrophil accumulation in Behcet's lesions.Publication Metadata only Increased CD4(+)CD16(+) and CD4(+)CD56(+) T cell subsets in Behcet's disease(SPRINGER VERLAG, 1999) DİRESKENELİ, RAFİ HANER; Eksioglu-Demiralp, E; Direskeneli, H; Ergun, T; Fresko, I; Akoglu, TBehcet's disease is a systemic vasculitis of unknown etiology. Various immune abnormalities have previously been shown in Behcet's disease. We investigated T lymphocyte subsets associated with cytotoxic activity and natural killer (NK) cells by flow cytometry in 37 patients with Behcet's disease, 38 healthy controls, and 17 diseased control patients. Compared to the healthy controls, CD4(+)CD16(+) and CD4(+)CD56(+) subsets were found to be higher in the Behcet's disease group as well as in the disease control group (CD4(+)CD16(+): B = 5 +/- 3, DC = 14 +/- 14, HC = 3 +/- 2, P = 0.001; CD4(+)CD56(+): ED = 11 +/- 5, DC = 18 +/- 17, HC = 8 +/- 6, P = 0.01). CD8(+)CD16(+) and CD8(+)CD56(+) T cell subsets were at normal levels in Behcet's disease but found to be elevated in disease controls. Similarly, NK cells (CD16(+)CD56(+)) were high only in the disease control group. Significant increases in CD4(+)CD16(+) and CD4(+)CD56(+) cell subsets in Behcet's patients and disease controls suggest that T cell activation patterns of these subsets in Behcet's disease are similar to those in other inflammatory disorders.