The W element is a positive regulator of HLA-DRA transcription in various DR+ cell types [published erratum appears in J Immunol 1991 May 1;146(9):3260-1]

• Published in: The Journal of immunology (1950) Vol. 146; no. 4; pp. 1361 - 1367
• Main Authors: Cogswell, JP, Austin, J, Ting, JP
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Am Assoc Immnol 15.02.1991; American Association of Immunologists
• Subjects: B-Lymphocytes - metabolism; Base Sequence; Biological and medical sciences; Cell Line; DNA-Binding Proteins - metabolism; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation - genetics; HLA-DR Antigens - genetics; Humans; Molecular and cellular biology; Molecular genetics; Molecular Sequence Data; Promoter Regions, Genetic; Regulatory Sequences, Nucleic Acid - physiology; Transcription, Genetic - genetics; Transcription. Transcription factor. Splicing. Rna processing; Human; Northern blotting; Regulation(control); Cell line; Transfection; Gene; Transcription; Major histocompatibility system; Class II histocompatibility antigen; Trans acting regulatory factor; B-Lymphocyte; DR-HLA-Locus
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.146.4.1361

The W and P elements are cis-acting transcriptional regulators of the human class II MHC gene HLA-DRA necessary for maximal promoter activity in DR+ B cells. Proteins that bind specifically to W may mediate promoter activity from a DNA segment containing W and P (W/P). In this report, we demonstrate that a -143 to -123 bp region that lacks P is sufficient to mediate the W elements function and to bind the W proteins W-B1 and W-B2 in the Raji B-lymphoblastoid cell line. In contrast to previous reports, we find that W/P is not a B cell-specific element; rather that its promoter activity parallels active transcription of the endogenous DRA gene. In addition, we show that tissue-restricted regulation by W/P is not correlated with the ubiquitous (W-B1) and lymphoid-specific (W-B2) distribution of the W binding proteins. We suggest that mechanisms in addition to binding to W may account for W/P-dependent transcriptional activation in DR+ cells.