HLA‐DQB1 Alleles May Influence the Surface Expression of DQ Molecules in Lymphomononuclear Cells of Type 1 Diabetes Mellitus Patients

To evaluate the expression of human leucocyte antigen (HLA) class II (DR and DQ) molecules on lymphomononuclear cells involved in the pathogenesis of type 1 diabetes, we studied 20 patients and 20 controls matched to patients for age, sex and HLA class II profile. The coexpression of HLA and CD3, CD...

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Veröffentlicht in:Scandinavian journal of immunology 2004-03, Vol.59 (3), p.305-309
Hauptverfasser: Fernandes, A. P. M., Foss, M. C., Donadi, E. A.
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Sprache:eng
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Zusammenfassung:To evaluate the expression of human leucocyte antigen (HLA) class II (DR and DQ) molecules on lymphomononuclear cells involved in the pathogenesis of type 1 diabetes, we studied 20 patients and 20 controls matched to patients for age, sex and HLA class II profile. The coexpression of HLA and CD3, CD4, CD8, CD19 and CD14 molecules was evaluated by flow cytometry. HLA‐DRB1, ‐DQA1 and ‐DQB1 alleles were assigned using amplified DNA hybridized with sequence‐specific primers. The fluorescence intensity of HLA‐DR and ‐DQ molecules observed on the surface of the lymphomononuclear cells of patients did not differ significantly from controls. Patients presented decreased percentage of double‐positive CD4+/DQ+ cells and increased percentage of CD19+/DR+ cells, irrespective of the HLA class II profile; however, the more dramatic alteration of the lymphomononuclear phenotype profile was observed for patients possessing the HLA‐DQB1*0201 allele. These patients exhibited decreased percentage of CD3+, CD4+, CD8+, CD19+ and CD14+ cells bearing HLA‐DQ molecules and decreased fluorescence intensity for HLA‐DQ molecules on CD19+ cells compared to patients without the DQB1*0201 allele. Although type 1 diabetes patients shared CD4/DQ or CD19/DR phenotype abnormalities, patients typed as DQB1*0201 presented additional abnormalities in terms of DQ expression and cell phenotypes bearing DQ molecules.
ISSN:0300-9475
1365-3083
DOI:10.1111/j.0300-9475.2004.01386.x