摘要：

The BCL-6 gene was cloned five years ago through its involvement in chromosomal translocations in non-Hodg kin's lymphomas. In normal lymphoid tissues, the highest BCL-6 expression is restricted to B cells and a subset of CD4+ T cells within germinal centers. In B-cell tumors, translocations deregulate the expression of BCL-6 by replacing its promoter with heterologous promoters, yet a normal BCL-6 protein is made which functions as se quence-specific transcription repressor. The 5' region of this gene has been found to be hypermutated in tumor as well as in normal germinal center B cells, presumably by the same mechanism responsible for immunoglobulin V region hypermutation. In BCL-6 knock out mice, T cell dependent B-cell responses are defective due to inability of these animals to develop germinal center. In addition, frequent occurrence of Th2 type inflammation also sug gests an important regulatory role of BCL-6 in cells of non-B lineage. Although the precise mechanism by which a deregulated BCL-6 gene contributes to lymphoma genesis is still not clear, expression of BCL-6 protein has been shown to be a very useful histogenetic marker in a variety of lymphoid malignancies.

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