Abstract
The large number of type I interferon genes in mammalian species could be explained by simple redundancy, by different functions for different interferons, or by different spatial or temporal patterns of expression. Different functions would require different receptors for each interferon, while different patterns of expression would require different transcriptional or postranscriptional regulatory mechanisms. It is also necessary to explain when and how this diversity was achieved. Information on comparative genetics of the interferon system, cloning of new interferon genes, studies on receptor interactions and studies on gene expression are accrued at each of the annual meetings of the ISICR. The last meeting held on October 2-7, 1994, at Budapest was not an exception, and this review summarizes some of this year's reports.
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