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Evidence for discoordinate regulation of the HLA-DPB1 gene
M T Coiras1, A M Alvarez-Barrientos, G Díaz
1Departmento de Microbiología II, Universidad Complutense, Madrid, Spain.
Characterization of cell lines derived from patients with type II bare lymphocyte syndrome, a pathological state in which the constitutive and inducible expression of HLA class II antigens is lacking, has permitted the identification of several trans-acting factors involved in the coordinated regulation of HLA class II genes. Although an increasing body of evidence has pointed to the existence of a discoordinate regulation of HLA class II loci, the mechanisms underlying such regulation are essentially unknown. In the present study, 45.EM2, a mutant lymphoblastoid cell line with a new pattern of HLA discoordinate expression is characterized. 45.EM2 expresses HLA-DR and -DQ but fails to express HLA-DP. The absence of HLA-DP expression in 45.EM2 is the result of a transcriptional defect, leading to a lack of DPB1 mRNA. By contrast, DPA1 transcription in this LCL is not impaired. The characteristics of 45.EM2 described here suggest the existence of a specific trans-acting factor involved in the control of DPB1 gene expression.
Characterization of cell lines derived from patients with type II bare lymphocyte syndrome, a pathological state in which the constitutive and inducible expression of HLA class II antigens is lacking, has permitted the identification of several trans-acting factors involved in the coordinated regulation of HLA class II genes. Although an increasing body of evidence has pointed to the existence of a discoordinate regulation of HLA class II loci, the mechanisms underlying such regulation are essentially unknown. In the present study, 45.EM2, a mutant lymphoblastoid cell line with a new pattern of HLA discoordinate expression is characterized. 45.EM2 expresses HLA-DR and -DQ but fails to express HLA-DP. The absence of HLA-DP expression in 45.EM2 is the result of a transcriptional defect, leading to a lack of DPB1 mRNA. By contrast, DPA1 transcription in this LCL is not impaired. The characteristics of 45.EM2 described here suggest the existence of a specific trans-acting factor involved in the control of DPB1 gene expression.