Publications

It has been a surprise to find that the two distinct subsets of mouse CD4+ T cells identified from clones cultured in vitro also occur during Leishmania infection. The spectrum of disease encountered during these infections ranges from successful resolution to fatal dissemination and in mice these outcomes are accompanied by expansion of TH1 or TH2 CD4+ cells, respectively. This review focuses on the mechanisms that cause such disparate responses to the parasite.

PP14 protein (placental protein 14) is abundantly secreted by the human endometrium under the influence of progesterone. Human PP14 is homologous to beta-lactoglobulin, the main component of equine, bovine, and ovine milk whey. A genomic PP14 probe (PP14G1) was used for the chromosome assignment of the PP14 gene. Somatic hybrid cells enabled PP14G1 to be assigned to chromosome 9. In situ hybridization further refined this assignment to 9q34. The localization of the PP14 gene in the region of the ABO locus is consistent with the linkage described in bovines between beta-lactoglobulin and the J blood group (homologous to the human ABO group).

HTLV-I structural gene expression is posttranscriptionally regulated by the Rex protein and the Rex response element (RexRE), a 255 nucleotide RNA stem-loop structure located in the retroviral 3' LTR. Independent of Rex, the RexRE also plays a critical role in the polyadenylation of all HTLV-I transcripts. Folding of the RexRE serves to spatially juxtapose the widely separated AAUAAA hexamer and GU-rich elements that are essential for polyadenylation. In turn, this folding promotes the cooperative and stable binding of two nuclear factors at these elements that commits this poly(A) site to 3' processing. These findings highlight a novel mechanism of 3' end formation in the HTLV family of retroviruses and underscore the general requirement for protein-protein interactions in the polyadenylation reaction.